脑型钠尿肽对神经系统细胞膜钾离子通道的调控和机制研究
|
摘要
钠尿肽家族是一个多肽类激素家族。该多肽以及其受体在生理和病理生理方面有着重要意义,涉及到肾脏系统、心血管系统、内分泌系统、神经系统和免疫系统等方面的调控,维持机体循环系统和内环境的稳定。众多的研究表明,钠尿肽可以调节许多离子通道。在神经系统中,钠尿肽作为一种神经肽,激活细胞膜上的受体蛋白从而引发多种生物效应。目前,有关脑型钠尿肽对神经系统离子通道的调控尚不清楚。我们选择神经系统两种细胞模型:Schwann细胞(胶质细胞)和小脑颗粒细胞(神经元),通过全细胞膜片钳记录,免疫组化和细胞增殖测试以及分子克隆技术,研究脑型钠尿肽(BNP)对这两种细胞模型上的延迟整流钾通道的调控机制,研究主要分以下三个部分:
第一部分:我们以取自小鼠坐骨神经和臂丛神经周围的Schwann细胞为胶质细胞模型,研究BNP对细胞膜钾电流以及细胞增殖的调制。通过全细胞膜片钳记录,我们发现BNP可增加Schwann细胞膜上TEA敏感的,I_K(延迟外向整流钾电流);在浓度为1 nM～500 nM范围内,这种增大作用具有部分浓度依赖性。同时,在100 nM BNP的作用下,I_K的半激活电位和半失活电位均发生左移。通过半定量PCR以及免疫组化鉴定,发现Schwann细胞表达A受体、B受体和C受体三种NP受体。先前的研究已表明BNP可与A受体和C受体结合,因此,我们使用NPR-A阻断剂和激动剂进行了涉及受体亚型的鉴定。实验结果揭示,给予200 nM anantin(NPR-A阻断剂)可抑制BNP的作用,而50 nM cANF(NPR-C特异性激动剂)无法模拟BNP的作用,提示BNP对于I_K的作用是通过NPR-A这一途径,而非NPR-C途径。细胞外给予50 gM 8-Br-cGMP可模拟BNP对I_K的增大作用,而细胞外给予100 gM db-cAMP则不能产生类似于BNP的效应。这些结果进一步提示BNP是通过A受体激动下游的cGMP通路,进而激活I_K。另外,我们将Schwann细胞在含有BNP的培养液中孵育五天,随后通过增殖检测和S100蛋白免疫组化标记,发现经BNP处理的Schwann细胞增殖能力有所增强。综上所述,神经肽BNP可增人Schwann细胞的I_K并对细胞增殖有一定的促进作用。BNP对于细胞增殖的促进作用,是否有钾通道这一途径的参与,还需进一步研究证实。这些研究有助于我们了解神经肽对于神经系统各层面的调控,以及胶质细胞自身的调控机制,并将这些研究应用于神经损伤治疗。
第二部分:我们在大鼠小脑颗粒细胞上研究BNP对细胞膜钾电流的调制。通过免疫组化鉴定,我们发现颗粒细胞上表达三种钠尿肽受体。通过全细胞膜片钳记录,我们发现BNP可减小颗粒细胞上TEA敏感的I_K;在浓度为10nM～1000nM范围内,这种增大作用具有部分浓度依赖性。同时,BNP可使小脑颗粒细胞I_K的半失活电位发生左移。给予200 nM anantin可抑制BNP的作用,而50 nM cANF无法模拟BNP的作用,提示BNP对于I_K的作用是通过NPR-A这一途径,而非NPR-C途径。细胞外给予50μM 8-Br-cGMP可模拟BNP对I_K的增大作用。这些结果进一步提示BNP通过A受体激动下游的cGMP通路降低I_K。BNP对颗粒细胞上钾电流的下调,可能参与调控神经细胞的兴奋性,以及与细胞的保护机制相关。
第三部分:BNP对Schwann细胞和小脑颗粒细胞上的延迟整流钾通道的调控途径相似,但是调控结果相反,可能是由于被调控的亚单位不同造成的。神经细胞中I_K的主要亚单位是Kv2.1α亚单位。我们使用Kv2.1α亚单位的特异性阻断剂JZTX-Ⅲ。1μM JZTX-Ⅲ存在时,BNP在颗粒细胞上对电流的抑制效果消失,电流幅度为原本的93.40±3.27%。而此时,BNP在Schwann细胞上对电流的增大效应依旧存在,增大46.24±1.45%,和Kv2.1α亚单位未被抑制时的电流增大率46.73±7.26%相比,无显著性差异。在颗粒细胞上BNP似乎仅对Kv2.1α亚单位有调控作用,而在Schwann细胞上Kv2.1α亚单位是BNP调控的一个对象之一。在转染了pmCherry-Kv2.1的HEK293细胞上,BNP无法调控Kv2.1α亚单位幅度,但可以调控通道的失活特性,这一调控与在颗粒细胞上表现一致。从Schwann细胞上克隆得到Kv1.2和Kv1.5α亚单位,转染到HEK293细胞上。结果发现BNP可上调Kv1.2α亚单位的幅度,下调Kv1.5α亚单位的幅度,并调控Kv1.2α亚单位的动力学特性。
In addition to natriuretic peptieds'roles in cardiovascular control and fluid volume regulation,a number of studies have revealed that NPs can modulate membrane ion channels.Brain natriuretic peptide may act as a neuromodulator via its associated receptors in the nervous system.However,few studies have reported on its activity on ion channels in the nervous system.
In this study,we chose two models of neurons and glia cells to study the effect of BNP on K~+ channels which are among the most diverse families of membrane proteins.Schwann cells are the satellite cell of the peripheral nervous system, responsible for myelination of nerve fibers in the peripheral nervous system. Voltage-dependent K~+ currents,including inactivating A-type currents(I_A), delayed-rectifier currents(I_K),and inward-rectifier currents(K_(IR)),constitute the main conductances found in SCs.Physiological studies have shown that I_K channels may play an important role in SC proliferation.Cerebellar granule neurons are widely used as a model to study neuronal fucntions.Primary cerebellar granule cells have been shown to possess various outward K_V currents,including outward transient K~+ current (I_A),outward rectifier delayed K~+ current(I_K),and the non-inactivating K~+ current I_(K(so)).
Here,we used the methods of patch-clamp recordings,immunocytochemistry and confocal microscopy,cell proliferation assays,DNA constructs and cell transfection to investigate the role of BNP in voltage-gated K~+ currents and detailed subunits in the nervous system.The research is divided into three parts as followings.
Part One:In this study,we determined that BNP upregulated the TEA-sensitive delayed rectifier outward potassium current(I_K) in mouse Schwann cells using whole-cell recording techniques.At concentrations of 1-500 nM,BNP reversibly activated I_K in a dose-dependent manner,with modulating its steady-state activation and inactivation properties.The effect of BNP on I_K was abolished by pre-incubation with the specific antagonist of NPR-A,and could not be mimicked by application of the NPR-C agonist.These results were supported by immunocytochemical findings indicating that NPR-A was abundantly expressed in Schwann cells.The application of 8-Br-cGMP mimicked the effect of BNP on I_K,but BNP was unable to further increase I_K after the application of 8-Br-cGMP.The effect of BNP on I_K was blocked by KT5823,an inhibitor of cGMP-dependent protein kinase(PKG).Genistein blocked I_K and also completely eliminated the effects of BNP and 8-Br-cGMP on I_K. Physiological studies have shown that I_K channels may play an important role in SC proliferation.BNP significantly stimulated Schwann cell proliferation and this effect could be partly inhibited by TEA.We therefore concluded that BNP modulated I_K via cGMP-and tyrosine kinase-dependent pathways by activation of NPR-A.This effect of BNP on I_K in Schwann cells might be involved in its effect on cell proliferation.
Part Two:In this study,we determined that BNP suppressed the TEA-sensitive delayed rectifier outward potassium current(I_K) in rat cerebellar granular cells using whole-cell recording techniques.At concentrations of 10-1000 nM,BNP reversibly activated I_K in a dose-dependent manner,with modulating its steady-inactivation properties.The effect of BNP on I_K was abolished by pre-incubation with the specific antagonist of NPR-A,and could not be mimicked by application of the NPR-C agonist.The application of 8-Br-cGMP mimicked the effect of BNP on I_K,but BNP was unable to further increase I_K after the application of 8-Br-cGMP.The effect of BNP on I_K was blocked by KT5823,an inhibitor of cGMP-dependent protein kinase (PKG).Moreover,incubation of isolated cell cultures in the BNP-containing medium also increased cGMP innunoreactivity in the granule cells.We therefore concluded that BNP modulated I_K via cGMP-PKG signal pathway by the activation of NPR-A.
Part Three:The effect of BNP on the amplitude of I_K was opposite on the Schwann cells and cerebellar granule cells,even through the similar signal pathway. This might result from different subunits regulated by BNP.Since Kv2.1 was the main a subunit of I_K on granule cells,we apply JZTX-Ⅲ,the specific blocker of Kv2.1,to inhibit Kv2.1αsubunit and then the effect of BNP on I_K was disappeared on granule cells.It seems that BNP effect Kv2.1αsubunit on granule cells.Besides,on the HEK293 cells transfected with pmCherry-Kv2.1,BNP could modulate the steady-inactivation property,similar to the modulation on native cerebellar granule cells.However,with the presence of JZTX-Ⅲ,the dominant effect of BNP could still be observed on Schwann cells,indicating that BNP might regulate other subunits on Schwann cells as well as Kv2.1αsubunit.Thus,we investigated the effect of BNP on the HEK293 cells transfected with pmCherry-Kv1.2 or pEGFP-Kv1.5.BNP could up-regulate the amplitude of Kv1.2αsubunit and down-regulate the amplitude of Kv1.5αsubunit.BNP could also modulate steady-state activation and inactivation properties of Kv1.2αsubunit,similar to the results observed in native Schwann cells.
第一部分:我们以取自小鼠坐骨神经和臂丛神经周围的Schwann细胞为胶质细胞模型,研究BNP对细胞膜钾电流以及细胞增殖的调制。通过全细胞膜片钳记录,我们发现BNP可增加Schwann细胞膜上TEA敏感的,I_K(延迟外向整流钾电流);在浓度为1 nM～500 nM范围内,这种增大作用具有部分浓度依赖性。同时,在100 nM BNP的作用下,I_K的半激活电位和半失活电位均发生左移。通过半定量PCR以及免疫组化鉴定,发现Schwann细胞表达A受体、B受体和C受体三种NP受体。先前的研究已表明BNP可与A受体和C受体结合,因此,我们使用NPR-A阻断剂和激动剂进行了涉及受体亚型的鉴定。实验结果揭示,给予200 nM anantin(NPR-A阻断剂)可抑制BNP的作用,而50 nM cANF(NPR-C特异性激动剂)无法模拟BNP的作用,提示BNP对于I_K的作用是通过NPR-A这一途径,而非NPR-C途径。细胞外给予50 gM 8-Br-cGMP可模拟BNP对I_K的增大作用,而细胞外给予100 gM db-cAMP则不能产生类似于BNP的效应。这些结果进一步提示BNP是通过A受体激动下游的cGMP通路,进而激活I_K。另外,我们将Schwann细胞在含有BNP的培养液中孵育五天,随后通过增殖检测和S100蛋白免疫组化标记,发现经BNP处理的Schwann细胞增殖能力有所增强。综上所述,神经肽BNP可增人Schwann细胞的I_K并对细胞增殖有一定的促进作用。BNP对于细胞增殖的促进作用,是否有钾通道这一途径的参与,还需进一步研究证实。这些研究有助于我们了解神经肽对于神经系统各层面的调控,以及胶质细胞自身的调控机制,并将这些研究应用于神经损伤治疗。
第二部分:我们在大鼠小脑颗粒细胞上研究BNP对细胞膜钾电流的调制。通过免疫组化鉴定,我们发现颗粒细胞上表达三种钠尿肽受体。通过全细胞膜片钳记录,我们发现BNP可减小颗粒细胞上TEA敏感的I_K;在浓度为10nM～1000nM范围内,这种增大作用具有部分浓度依赖性。同时,BNP可使小脑颗粒细胞I_K的半失活电位发生左移。给予200 nM anantin可抑制BNP的作用,而50 nM cANF无法模拟BNP的作用,提示BNP对于I_K的作用是通过NPR-A这一途径,而非NPR-C途径。细胞外给予50μM 8-Br-cGMP可模拟BNP对I_K的增大作用。这些结果进一步提示BNP通过A受体激动下游的cGMP通路降低I_K。BNP对颗粒细胞上钾电流的下调,可能参与调控神经细胞的兴奋性,以及与细胞的保护机制相关。
第三部分:BNP对Schwann细胞和小脑颗粒细胞上的延迟整流钾通道的调控途径相似,但是调控结果相反,可能是由于被调控的亚单位不同造成的。神经细胞中I_K的主要亚单位是Kv2.1α亚单位。我们使用Kv2.1α亚单位的特异性阻断剂JZTX-Ⅲ。1μM JZTX-Ⅲ存在时,BNP在颗粒细胞上对电流的抑制效果消失,电流幅度为原本的93.40±3.27%。而此时,BNP在Schwann细胞上对电流的增大效应依旧存在,增大46.24±1.45%,和Kv2.1α亚单位未被抑制时的电流增大率46.73±7.26%相比,无显著性差异。在颗粒细胞上BNP似乎仅对Kv2.1α亚单位有调控作用,而在Schwann细胞上Kv2.1α亚单位是BNP调控的一个对象之一。在转染了pmCherry-Kv2.1的HEK293细胞上,BNP无法调控Kv2.1α亚单位幅度,但可以调控通道的失活特性,这一调控与在颗粒细胞上表现一致。从Schwann细胞上克隆得到Kv1.2和Kv1.5α亚单位,转染到HEK293细胞上。结果发现BNP可上调Kv1.2α亚单位的幅度,下调Kv1.5α亚单位的幅度,并调控Kv1.2α亚单位的动力学特性。
In addition to natriuretic peptieds'roles in cardiovascular control and fluid volume regulation,a number of studies have revealed that NPs can modulate membrane ion channels.Brain natriuretic peptide may act as a neuromodulator via its associated receptors in the nervous system.However,few studies have reported on its activity on ion channels in the nervous system.
In this study,we chose two models of neurons and glia cells to study the effect of BNP on K~+ channels which are among the most diverse families of membrane proteins.Schwann cells are the satellite cell of the peripheral nervous system, responsible for myelination of nerve fibers in the peripheral nervous system. Voltage-dependent K~+ currents,including inactivating A-type currents(I_A), delayed-rectifier currents(I_K),and inward-rectifier currents(K_(IR)),constitute the main conductances found in SCs.Physiological studies have shown that I_K channels may play an important role in SC proliferation.Cerebellar granule neurons are widely used as a model to study neuronal fucntions.Primary cerebellar granule cells have been shown to possess various outward K_V currents,including outward transient K~+ current (I_A),outward rectifier delayed K~+ current(I_K),and the non-inactivating K~+ current I_(K(so)).
Here,we used the methods of patch-clamp recordings,immunocytochemistry and confocal microscopy,cell proliferation assays,DNA constructs and cell transfection to investigate the role of BNP in voltage-gated K~+ currents and detailed subunits in the nervous system.The research is divided into three parts as followings.
Part One:In this study,we determined that BNP upregulated the TEA-sensitive delayed rectifier outward potassium current(I_K) in mouse Schwann cells using whole-cell recording techniques.At concentrations of 1-500 nM,BNP reversibly activated I_K in a dose-dependent manner,with modulating its steady-state activation and inactivation properties.The effect of BNP on I_K was abolished by pre-incubation with the specific antagonist of NPR-A,and could not be mimicked by application of the NPR-C agonist.These results were supported by immunocytochemical findings indicating that NPR-A was abundantly expressed in Schwann cells.The application of 8-Br-cGMP mimicked the effect of BNP on I_K,but BNP was unable to further increase I_K after the application of 8-Br-cGMP.The effect of BNP on I_K was blocked by KT5823,an inhibitor of cGMP-dependent protein kinase(PKG).Genistein blocked I_K and also completely eliminated the effects of BNP and 8-Br-cGMP on I_K. Physiological studies have shown that I_K channels may play an important role in SC proliferation.BNP significantly stimulated Schwann cell proliferation and this effect could be partly inhibited by TEA.We therefore concluded that BNP modulated I_K via cGMP-and tyrosine kinase-dependent pathways by activation of NPR-A.This effect of BNP on I_K in Schwann cells might be involved in its effect on cell proliferation.
Part Two:In this study,we determined that BNP suppressed the TEA-sensitive delayed rectifier outward potassium current(I_K) in rat cerebellar granular cells using whole-cell recording techniques.At concentrations of 10-1000 nM,BNP reversibly activated I_K in a dose-dependent manner,with modulating its steady-inactivation properties.The effect of BNP on I_K was abolished by pre-incubation with the specific antagonist of NPR-A,and could not be mimicked by application of the NPR-C agonist.The application of 8-Br-cGMP mimicked the effect of BNP on I_K,but BNP was unable to further increase I_K after the application of 8-Br-cGMP.The effect of BNP on I_K was blocked by KT5823,an inhibitor of cGMP-dependent protein kinase (PKG).Moreover,incubation of isolated cell cultures in the BNP-containing medium also increased cGMP innunoreactivity in the granule cells.We therefore concluded that BNP modulated I_K via cGMP-PKG signal pathway by the activation of NPR-A.
Part Three:The effect of BNP on the amplitude of I_K was opposite on the Schwann cells and cerebellar granule cells,even through the similar signal pathway. This might result from different subunits regulated by BNP.Since Kv2.1 was the main a subunit of I_K on granule cells,we apply JZTX-Ⅲ,the specific blocker of Kv2.1,to inhibit Kv2.1αsubunit and then the effect of BNP on I_K was disappeared on granule cells.It seems that BNP effect Kv2.1αsubunit on granule cells.Besides,on the HEK293 cells transfected with pmCherry-Kv2.1,BNP could modulate the steady-inactivation property,similar to the modulation on native cerebellar granule cells.However,with the presence of JZTX-Ⅲ,the dominant effect of BNP could still be observed on Schwann cells,indicating that BNP might regulate other subunits on Schwann cells as well as Kv2.1αsubunit.Thus,we investigated the effect of BNP on the HEK293 cells transfected with pmCherry-Kv1.2 or pEGFP-Kv1.5.BNP could up-regulate the amplitude of Kv1.2αsubunit and down-regulate the amplitude of Kv1.5αsubunit.BNP could also modulate steady-state activation and inactivation properties of Kv1.2αsubunit,similar to the results observed in native Schwann cells.
引文
[1] DE BOLD A J, BORENSTEIN H B, VERESS A T, et al. A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats [J]. Life Sci, 1981, 28(1):89-94.
[2] SUDOH T, KANGAWA K, MINAMINO N, et al. A new natriuretic peptide in porcine brain [J]. Nature, 1988, 332(6159): 78-81.
[3] SUDOH T, MINAMINO N, KANGAWA K, et al. C-type natriuretic peptide (CNP): a new member of natriuretic peptide family identified in porcine brain [J]. Biochem Biophys Res Commun, 1990, 168(2): 863-70.
[4] DICICCO-BLOOM E, LELIEVRE V, ZHOU X, et al. Embryonic expression and multifunctional actions of the natriuretic peptides and receptors in the developing nervous system [J]. Dev Biol, 2004, 271(1): 161-75.
[5] INOHA S, INAMURA T, NAKAMIZO A, et al. Fluid loading in rats increases serum brain natriuretic peptide concentration [J]. Neurol Res, 2001, 23(1): 93-5.
[6] DE BOLD A J, DE BOLD M L. Determinants of natriuretic peptide production by the heart: basic and clinical implications [J]. J Investig Med, 2005, 53(7): 371-7.
[7] SVIRI G E, SHIK V, RAZ B, et al. Role of brain natriuretic peptide in cerebral vasospasm [J]. Acta Neurochir(Wien), 2003, 145(10): 851-60; discussion 60.
[8] BIGGIN P C, ROOSILD T, CHOE S. Potassium channel structure: domain by domain [J]. Curr Opin Struct Biol, 2000, 10(4): 456-61.
[9] DAI S, HALL D D, HELL J W. Supramolecular assemblies and localized regulation of voltage-gated ion channels [J]. Physiol Rev, 2009, 89(2): 411-52.
[10] Molecular and Functional Diversity of Ion Channels and Receptors. Proceedings of a conference. New York City, New York, USA. May 14-17, 1998 [J]. Ann N Y Acad Sci, 1999,868(1-774.
[11] RETTIG J, HEINEMANN S H, WUNDER F, et al. Inactivation properties of voltage-gated K+ channels altered by presence of beta-subunit [J]. Nature, 1994, 369(6478): 289-94.
[12] SHI G, NAKAHIRA K, HAMMOND S, et al. Beta subunits promote K+ channel surface expression through effects early in biosynthesis [J]. Neuron, 1996, 16(4): 843-52.
[13] NAGAYA N, PAPAZIAN D M. Potassium channel alpha and beta subunits assemble in the endoplasmic reticulum [J]. J Biol Chem, 1997, 272(5): 3022-7.
[14] YU Y C, CAO L H, YANG X L. Modulation by brain natriuretic peptide of GABA receptors on rat retinal ON-type bipolar cells [J]. J Neurosci, 2006, 26(2): 696-707.
[15] XU H Y, HUANG X, YANG M, et al. The effect of C-type natriuretic peptide on delayed rectifier potassium currents in gastric antral circular myocytes of the guinea-pig [J]. Physiol Res,2008, 57(1): 55-62.
[16] TANAKA Y, TANG G, TAKIZAWA K, et al. Kv channels contribute to nitric oxide- and atrial natriuretic peptide-induced relaxation of a rat conduit artery [J]. J Pharmacol Exp Ther, 2006,317(1):341-54.
[17] FAGNI L, BOSSU J L, BOCKAERT J. Activation of a Large-conductance Ca2+-Dependent K+ Channel by Stimulation of Glutamate Phosphoinositide-coupled Receptors in Cultured Cerebellar Granule Cells [J]. Eur J Neurosci, 1991, 3(8): 778-89.
[18] WATKINS C S, MATHIE A. Modulation of the gating of the transient outward potassium current of rat isolated cerebellar granule neurons by lanthanum [J]. Pflugers Arch, 1994, 428(3-4): 209-16.
[19] WATKINS C S, MATHIE A. A non-inactivating K+ current sensitive to muscarinic receptor activation in rat cultured cerebellar granule neurons [J]. J Physiol, 1996,491 (Pt 2)(401-12.
[20] HU C L, LIU Z, GAO Z Y, et al. 2-iodomelatonin prevents apoptosis of cerebellar granule neurons via inhibition of A-type transient outward K+ currents [J]. J Pineal Res, 2005, 38(1):53-61.
[21] JIAO S, WU M M, HU C L, et al. Melatonin receptor agonist 2-iodomelatonin prevents apoptosis of cerebellar granule neurons via K(+) current inhibition [J]. J Pineal Res, 2004, 36(2):109-16.
[22] LIU L Y, HOFFMAN G E, FEI X W, et al. Delayed rectifier outward K+ current mediates the migration of rat cerebellar granule cells stimulated by melatonin [J]. J Neurochem, 2007, 102(2):333-44.
[23] VACHER H, MOHAPATRA D P, TRIMMER J S. Localization and targeting of voltage-dependent ion channels in mammalian central neurons [J]. Physiol Rev, 2008, 88(4):1407-47.
[24] FROSTICK S P, YIN Q, KEMP G J. Schwann cells, neurotrophic factors, and peripheral nerve regeneration [J]. Microsurgery, 1998, 18(7): 397-405.
[25] BAKER M D. Electrophysiology of mammalian Schwann cells [J]. Prog Biophys Mol Biol, 2002, 78(2-3): 83-103.
[26] SOBKO A, PERETZ A, SHIR1HAI O, et al. Heteromultimeric delayed-rectifier K+ channels in schwann cells: developmental expression and role in cell proliferation [J]. J Neurosci, 1998, 18(24): 10398-408.
[27] MI H, DEERINCK T J, ELLISMAN M H, et al. Differential distribution of closely related potassium channels in rat Schwann cells [J]. J Neurosci, 1995, 15(5 Pt 2): 3761-74.
[28] WILSON G F, CHIU S Y. Potassium channel regulation in Schwann cells during early developmental myelinogenesis [J]. J Neurosci, 1990, 10(5): 1615-25.
[29] PERETZ A, SOBKO A, ATTALI B. Tyrosine kinases modulate K+ channel gating in mouse Schwann cells [J]. J Physiol, 1999, 519 Pt 2(373-84.
[30] ROOTS B I. Comparative studies on glial markers [J]. J Exp Biol, 1981, 95(167-80.
[31] YUAN C, YANG S, LIAO Z, et al. Effects and mechanism of Chinese tarantula toxins on the Kv2.1 potassium channels [J]. Biochem Biophys Res Commun, 2007, 352(3): 799-804.
[32] HIRSCH J, SCHLATTER E. Genistein potentiates the ANP effect on a K(+)-conductance in HEK-293 cells [J]. Cell Physiol Biochem, 2003, 13(4): 223-8.
[33] AIRHART N, YANG Y F, ROBERTS C T, JR., et al. Atrial natriuretic peptide induces natriuretic peptide receptor-cGMP-dependent protein kinase interaction [J]. J Biol Chem, 2003,278(40): 38693-8.
[34] NITABACH M N, LLAMAS D A, THOMPSON I J, et al. Phosphorylation-dependent and phosphorylation-independent modes of modulation of shaker family voltage-gated potassium channels by SRC family protein tyrosine kinases [J]. J Neurosci, 2002, 22(18): 7913-22.
[35] SOBKO A, PERETZ A, ATTALI B. Constitutive activation of delayed-rectifier potassium channels by a src family tyrosine kinase in Schwann cells [J]. Embo J, 1998, 17(16): 4723-34.
[36] LELIEVRE V, PINEAU N, HU Z, et al. Proliferative actions of natriuretic peptides on neuroblastoma cells. Involvement of guanylyl cyclase and non-guanylyl cyclase pathways [J]. J Biol Chem, 2001, 276(47): 43668-76.
[37] DE BOLD A J. Atrial natriuretic factor: a hormone produced by the heart [J]. Science, 1985, 230(4727): 767-70.
[38] NAPIER M A, DEWEY R S, ALBERS-SCHONBERG G, et al. Isolation and sequence determination of peptide components of atrial natriuretic factor [J]. Biochem Biophys Res Commun, 1984, 120(3): 981-8.
[39] MISONO K S, GRAMMER R T, FUKUMI H, et al. Rat atrial natriuretic factor: isolation, structure and biological activities of four major peptides [J]. Biochem Biophys Res Commun,1984, 123(2): 444-51.
[40] FLYNN T G, DE BOLD M L, DE BOLD A J. The amino acid sequence of an atrial peptide with potent diuretic and natriuretic properties [J]. Biochem Biophys Res Commun, 1983, 117(3):859-65.
[41] CURRIE M G, GELLER D M, COLE B R, et al. Purification and sequence analysis of bioactive atrial peptides (atriopeptins) [J]. Science, 1984, 223(4631): 67-9.
[42] KANGAWA K, TAWARAGI Y, OIKAWA S, et al. Identification of rat gamma atrial natriuretic polypeptide and characterization of the cDNA encoding its precursor [J]. Nature, 1984,312(5990): 152-5.
[43] MCGRATH M F, DE BOLD A J. Determinants of natriuretic peptide gene expression [J]. Peptides, 2005, 26(6): 933-43.
[44] TAKEI Y. Structural and functional evolution of the natriuretic peptide system in vertebrates [J]. Int Rev Cytol, 2000, 194(1-66.
[45] INOUE K, NARUSE K, YAMAGAMI S, et al. Four functionally distinct C-type natriuretic peptides found in fish reveal evolutionary history of the natriuretic peptide system [J]. Proc Natl Acad Sci U S A, 2003, 100(17): 10079-84.
[46] GUTKOWSKA J, NEMER M. Structure, expression, and function of atrial natriuretic factor in extraatrial tissues [J]. Endocr Rev, 1989, 10(4): 519-36.
[47] GU J, D'ANDREA M, SEETHAPATHY M. Atrial natriuretic peptide and its messenger ribonucleic acid in overloaded and overload-released ventricles of rat [J]. Endocrinology, 1989,125(4): 2066-74.
[48] SA1TO Y, NAKAO K, ARAI H, et al. Augmented expression of atrial natriuretic polypeptide gene in ventricle of human failing heart [J]. J Clin Invest, 1989, 83(1): 298-305.
[49] STASCH J P, HIRTH-DIETRICH C, KAZDA S, et al. Endothelin stimulates release of atrial natriuretic peptides in vitro and in vivo [J]. Life Sci, 1989, 45(10): 869-75.
[50] SOUALMIA H, BARTHELEMY C, MASSON F, et al. Angiotensin Ⅱ-induced phosphoinositide production and atrial natriuretic peptide release in rat atrial tissue [J]. J Cardiovasc Pharmacol, 1997, 29(5): 605-11.
[51] LACHANCE D, GARCIA R, GUTKOWSKA J, et al. Mechanisms of release of atrial natriuretic factor. I. Effect of several agonists and steroids on its release by atrial minces [J].Biochem Biophys Res Commun, 1986, 135(3): 1090-8.
[52] THIBAULT G, AMIRI F, GARCIA R. Regulation of natriuretic peptide secretion by the heart [J]. Annu Rev Physiol, 1999, 61(193-217.
[53] EDWARDS B S, ZIMMERMAN R S, SCHWAB T R, et al. Atrial stretch, not pressure, is the principal determinant controlling the acute release of atrial natriuretic factor [J]. Circ Res, 1988, 62(2): 191-5.
[54] CODY R J, ATLAS S A, LARAGH J H, et al. Atrial natriuretic factor in normal subjects and heart failure patients. Plasma levels and renal, hormonal, and hemodynamic responses to peptide infusion [J]. J Clin Invest, 1986, 78(5): 1362-74.
[55] YANG-FENG T L, FLOYD-SMITH G, NEMER M, et al. The pronatriodilatin gene is located on the distal short arm of human chromosome 1 and on mouse chromosome 4 [J]. Am J Hum Genet, 1985, 37(6): 1117-28.
[56] MAKI M, TAKAYANAGI R, MISONO K S, et al. Structure of rat atrial natriuretic factor precursor deduced from cDNA sequence [J]. Nature, 1984, 309(5970): 722-4.
[57] YAMANAKA M, GREENBERG B, JOHNSON L, et al. Cloning and sequence analysis of the cDNA for the rat atrial natriuretic factor precursor [J]. Nature, 1984, 309(5970): 719-22.
[58] YAN W, WU F, MORSER J, et al. Corin, a transmembrane cardiac serine protease, acts as a pro-atrial natriuretic peptide-converting enzyme [J]. Proc Natl Acad Sci U S A, 2000, 97(15):8525-9.
[59] CHAN J C, KNUDSON O, WU F, et al. Hypertension in mice lacking the proatrial natriuretic peptide convertase corin [J]. Proc Natl Acad Sci U S A, 2005, 102(3): 785-90.
[60] WU F, YAN W, PAN J, et al. Processing of pro-atrial natriuretic peptide by corin in cardiac myocytes [J]. J Biol Chem, 2002, 277(19): 16900-5.
[61] GARDNER D G, CHEN S, GLENN D J, et al. Molecular biology of the natriuretic peptide system: implications for physiology and hypertension [J]. Hypertension, 2007, 49(3): 419-26.
[62] SCHULZ-KNAPPE P, FORSSMANN K, HERBST F, et al. Isolation and structural analysis of "urodilatin", a new peptide of the cardiodilatin-(ANP)-family, extracted from human urine [J].Klin Wochenschr, 1988, 66(17): 752-9.
[63] FORSSMANN W G, RICHTER R, MEYER M. The endocrine heart and natriuretic peptides: histochemistry, cell biology, and functional aspects of the renal urodilatin system [J]. Histochem Cell Biol, 1998, 110(4): 335-57.
[64] MUKOYAMA M, NAKAO K, HOSODA K, et al. Brain natriuretic peptide as a novel cardiac hormone in humans. Evidence for an exquisite dual natriuretic peptide system, atrial natriuretic peptide and brain natriuretic peptide [J]. J Clin Invest, 1991, 87(4): 1402-12.
[65] GREPIN C, DAGN1NO L, ROBITAILLE L, et al. A hormone-encoding gene identifies a pathway for cardiac but not skeletal muscle gene transcription [J]. Mol Cell Biol, 1994, 14(5): 3115-29.
[66] THUERAUF D J, HANFORD D S, GLEMBOTSKI C C. Regulation of rat brain natriuretic peptide transcription. A potential role for G ATA-related transcription factors in myocardial cell gene expression [J]. J Biol Chem, 1994, 269(27): 17772-5.
[67] TOGASHI K, ANDO K, HASEGAWA N, et al. Concentrations of brain natriuretic peptide in treated congestive heart failure [J]. Clin Chem, 1991, 37(5): 765.
[68] TAMURA N, OGAWA Y, CHUSHO H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide [J]. Proc Natl Acad Sci U S A, 2000,97(8): 4239-44.
[69] SEILHAMER J J, ARFSTEN A, MILLER J A, et al. Human and canine gene homologs of porcine brain natriuretic peptide [J]. Biochem Biophys Res Commun, 1989, 165(2): 650-8.
[70] SUDOH T, MINAMINO N, KANGAWA K, et al. Brain natriuretic peptide-32: N-terminal six amino acid extended form of brain natriuretic peptide identified in porcine brain [J]. Biochem Biophys Res Commun, 1988, 155(2): 726-32.
[71] OGAWA Y, ITOH H, TAMURA N, et al. Molecular cloning of the complementary DNA and gene that encode mouse brain natriuretic peptide and generation of transgenic mice that overexpress the brain natriuretic peptide gene [J]. J Clin Invest, 1994, 93(5): 1911-21.
[72] KOJIMA M, MINAMINO N, KANGAWA K, et al. Cloning and sequence analysis of cDNA encoding a precursor for rat brain natriuretic peptide [J]. Biochem Biophys Res Commun, 1989, 159(3): 1420-6.
[73] SUDOH T, MAEKAWA K, KOJIMA M, et al. Cloning and sequence analysis of cDNA encoding a precursor for human brain natriuretic peptide [J]. Biochem Biophys Res Commun,1989, 159(3): 1427-34.
[74] HAGIWARA H, SAKAGUCHI H, ITAKURA M, et al. Autocrine regulation of rat chondrocyte proliferation by natriuretic peptide C and its receptor, natriuretic peptide receptor-B [J]. J Biol Chem, 1994, 269(14): 10729-33.
[75] HAGIWARA H, SAKAGUCHI H, LODHI K M, et al. Subtype switching of natriuretic peptide receptors in rat chondrocytes during in vitro culture [J]. J Biochem, 1994, 116(3): 606-9.
[76] SUGA S, NAKAO K, ITOH H, et al. Endothelial production of C-type natriuretic peptide and its marked augmentation by transforming growth factor-beta. Possible existence of "vascular natriuretic peptide system" [J]. J Clin Invest, 1992, 90(3): 1145-9.
[77] SUGA S, ITOH H, KOMATSU Y, et al. Cytokine-induced C-type natriuretic peptide (CNP) secretion from vascular endothelial cells-evidence for CNP as a novel autocrine/paracrine regulator from endothelial cells [J]. Endocrinology, 1993, 133(6): 3038-41.
[78] IGAKI T, ITOH H, SUGA S, et al. Insulin suppresses endothelial secretion of C-type natriuretic peptide, a novel endothelium-derived relaxing peptide [J]. Diabetes, 1996, 45 Suppl 3(S62-4.
[79] KALRA P R, CLAGUE J R, BOLGER A P, et al. Myocardial production of C-type natriuretic peptide in chronic heart failure [J]. Circulation, 2003, 107(4): 571-3.
[80] WEI C M, HEUBLEIN D M, PERRELLA M A, et al. Natriuretic peptide system in human heart failure [J]. Circulation, 1993, 88(3): 1004-9.
[81] CHUSHO H, TAMURA N, OGAWA Y, et al. Dwarfism and early death in mice lacking C-type natriuretic peptide [J]. Proc Natl Acad Sci U S A, 2001, 98(7): 4016-21.
[82] NAKAYAMA T. The genetic contribution of the natriuretic peptide system to cardiovascular diseases [J]. Endocr J, 2005, 52(1): 11-21.
[83] OGAWA Y, ITOH H, YOSHITAKE Y, et al. Molecular cloning and chromosomal assignment of the mouse C-type natriuretic peptide (CNP) gene (Nppc): comparison with the human CNP gene (NPPC) [J]. Genomics, 1994, 24(2): 383-7.
[84] OGAWA Y, NAKAO K, NAKAGAWA O, et al. Human C-type natriuretic peptide. Characterization of the gene and peptide [J]. Hypertension, 1992, 19(6 Pt 2): 809-13.
[85] WU C, WU F, PAN J, et al. Furin-mediated processing of Pro-C-type natriuretic peptide [J]. J Biol Chem, 2003, 278(28): 25847-52.
[86] YEUNG V T, HO S K, NICHOLLS M G, et al. Binding of CNP-22 and CNP-53 to cultured mouse astrocytes and effects on cyclic GMP [J]. Peptides, 1996, 17(1): 101-6.
[87] TAWARAGI Y, FUCH1MURA K, TANAKA S, et al. Gene and precursor structures of human C-type natriuretic peptide [J]. Biochem Biophys Res Commun, 1991, 175(2): 645-51.
[88] TOTSUNE K, TAKAHASHI K, OHNEDA M, et al. C-type natriuretic peptide in the human central nervous system: distribution and molecular form [J]. Peptides, 1994, 15(1): 37-40.
[89] STINGO A J, CLAVELL A L, HEUBLEIN D M, et al. Presence of C-type natriuretic peptide in cultured human endothelial cells and plasma [J]. Am J Physiol, 1992, 263(4 Pt 2): H1318-21.
[90] MINAMINO N, MAKINO Y, TATEYAMA H, et al. Characterization of immunoreactive human C-type natriuretic peptide in brain and heart [J]. Biochem Biophys Res Commun, 1991,179(1): 535-42.
[91] TOGASHI K, KAMEYA T, KUROSAWA T, et al. Concentrations and molecular forms of C-type natriuretic peptide in brain and cerebrospinal fluid [J]. Clin Chem, 1992, 38(10): 2136-9.
[92] GREENBERG R N, HILL M, CRYTZER J, et al. Comparison of effects of uroguanylin, guanylin, and Escherichia coli heat-stable enterotoxin STa in mouse intestine and kidney:evidence that uroguanylin is an intestinal natriuretic hormone [J]. J Investig Med, 1997, 45(5): 276-82.
[93] SCHWEITZ H, VIGNE P, MOINIER D, et al. A new member of the natriuretic peptide family is present in the venom of the green mamba (Dendroaspis angusticeps) [J]. J Biol Chem, 1992, 267(20): 13928-32.
[94] LISY O, JOUGASAKI M, HEUBLEIN D M, et al. Renal actions of synthetic dendroaspis natriuretic peptide [J]. Kidney Int, 1999, 56(2): 502-8.
[95] THOMAS G, MOFFATT P, SALOIS P, et al. Osteocrin, a novel bone-specific secreted protein that modulates the osteoblast phenotype [J]. J Biol Chem, 2003,278(50): 50563-71.
[96] NISHIZAWA H, MATSUDA M, YAMADA Y, et al. Musclin, a novel skeletal muscle-derived secretory factor [J]. J Biol Chem, 2004, 279(19): 19391-5.
[97] MOFFATT P, THOMAS G, SELLIN K, et al. Osteocrin is a specific ligand of the natriuretic Peptide clearance receptor that modulates bone growth [J]. J Biol Chem, 2007, 282(50): 36454-62.
[98] LOWE D G, CHANG M S, HELLMISS R, et al. Human atrial natriuretic peptide receptor defines a new paradigm for second messenger signal transduction [J]. Embo J, 1989, 8(5):1377-84.
[99] SCHULZ S, SINGH S, BELLET R A, et al. The primary structure of a plasma membrane guanylate cyclase demonstrates diversity within this new receptor family [J]. Cell, 1989, 58(6):1155-62.
[100] NAGASE M, KATAFUCHI T, HIROSE S, et al. Tissue distribution and localization of natriuretic peptide receptor subtypes in stroke-prone spontaneously hypertensive rats [J]. J Hypertens, 1997, 15(11): 1235-43.
[101] WILCOX J N, AUGUSTINE A, GOEDDEL D V, et al. Differential regional expression of three natriuretic peptide receptor genes within primate tissues [J]. Mol Cell Biol, 1991, 11(7):3454-62.
[102] HERMAN J P, DOLGAS C M, RUCKER D, et al. Localization of natriuretic peptide-activated guanylate cyclase mRNAs in the rat brain [J]. J Comp Neurol, 1996, 369(2): 165-87.
[103] LANGUB M C, JR., DOLGAS C M, WATSON R E, JR., et al. The C-type natriuretic peptide receptor is the predominant natriuretic peptide receptor mRNA expressed in rat hypothalamus [J]. J Neuroendocrinol, 1995,7(4): 305-9.
[104] POTTER L R, HUNTER T. Phosphorylation of the kinase homology domain is essential for activation of the A-type natriuretic peptide receptor [J]. Mol Cell Biol, 1998, 18(4): 2164-72.
[105] FETHIERE J, GRAIHLE R, LAROSE L, et al. Distribution and regulation of natriuretic factor-RlC receptor subtypes in mammalian cell lines [J]. Mol Cell Biochem, 1993, 124(1): 11-6.
[106] POTTER L R, HUNTER T. Guanylyl cyclase-linked natriuretic peptide receptors: structure and regulation [J]. J Biol Chem, 2001, 276(9): 6057-60.
[107] POTTER L R. Domain analysis of human transmembrane guanylyl cyclase receptors: implications for regulation [J]. Front Biosci, 2005, 10(1205-20.
[108] SUGA S, NAKAO K, HOSODA K, et al. Receptor selectivity of natriuretic peptide family, atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide [J].Endocrinology, 1992, 130(1): 229-39.
[109] TAKAHASHI Y, NAKAYAMA T, SOMA M, et al. Organization of the human natriuretic peptide receptor A gene [J]. Biochem Biophys Res Commun, 1998, 246(3): 736-9.
[110] YAMAGUCH1 M, RUTLEDGE L J, GARBERS D L. The primary structure of the rat guanylyl cyclase A/atrial natriuretic peptide receptor gene [J]. J Biol Chem, 1990, 265(33):20414-20.
[111] LOPEZ M J, WONG S K, K1SHIMOTO I, et al. Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide [J]. Nature, 1995, 378(6552):65-8.
[112] OLIVER P M, FOX J E, KIM R, et al. Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A [J]. Proc Natl Acad Sci U S A, 1997, 94(26):14730-5.
[113] CHRISMAN T D, SCHULZ S, POTTER L R, et al. Seminal plasma factors that cause large elevations in cellular cyclic GMP are C-type natriuretic peptides [J]. J Biol Chem, 1993, 268(5): 3698-703.
[114] KOLLER K J, GOEDDEL D V. Molecular biology of the natriuretic peptides and their receptors [J]. Circulation, 1992, 86(4): 1081-8.
[115] REHEMUDULA D, NAKAYAMA T, SOMA M, et al. Structure of the type B human natriuretic peptide receptor gene and association of a novel microsatellite polymorphism with essential hypertension [J]. Circ Res, 1999, 84(5): 605-10.
[116] BARTELS C F, BUKULMEZ H, PADAYATTI P, et al. Mutations in the transmembrane natriuretic peptide receptor NPR-B impair skeletal growth and cause acromesomelic dysplasia, type Maroteaux [J]. Am J Hum Genet, 2004, 75(1): 27-34.
[117] PORTER J G, ARFSTEN A, FULLER F, et al. Isolation and functional expression of the human atrial natriuretic peptide clearance receptor cDNA [J]. Biochem Biophys Res Commun,1990, 171(2): 796-803.
[118] VAN DEN AKKER F. Structural insights into the ligand binding domains of membrane bound guanylyl cyclases and natriuretic peptide receptors [J]. J Mol Biol, 2001, 311(5): 923-37.
[119] FULLER F, PORTER J G, ARFSTEN A E, et al. Atrial natriuretic peptide clearance receptor. Complete sequence and functional expression of cDNA clones [J]. J Biol Chem, 1988, 263(19):9395-401.
[120] STULTS J T, O'CONNELL K L, GARCIA C, et al. The disulfide linkages and glycosylation sites of the human natriuretic peptide receptor-C homodimer [J]. Biochemistry, 1994, 33(37):11372-81.
[121] ITAKURA M, IWASHINA M, MIZUNO T, et al. Mutational analysis of disulfide bridges in the type C atrial natriuretic peptide receptor [J]. J Biol Chem, 1994, 269(11): 8314-8.
[122] MAACK T, SUZUKI M, ALMEIDA F A, et al. Physiological role of silent receptors of atrial natriuretic factor [J]. Science, 1987, 238(4827): 675-8.
[123] HE X L, DUKKIPATI A, WANG X, et al. A new paradigm for hormone recognition and allosteric receptor activation revealed from structural studies of NPR-C [J]. Peptides, 2005, 26(6):1035-43.
[124] RAHMUTULA D, NAKAYAMA T, SOMA M, et al. Structure and polymorphisms of the human natriuretic peptide receptor C gene [J]. Endocrine, 2002, 17(2): 85-90.
[125] CHINKERS M, WILSON E M. Ligand-independent oligomerization of natriuretic peptide receptors. Identification of heteromeric receptors and a dominant negative mutant [J]. J Biol Chem,1992,267(26): 18589-97.
[126] IWATA T, UCHIDA-MIZUNO K, KATAFUCHI T, et al. Bifunctional atrial natriuretic peptide receptor (type A) exists as a disulfide-linked tetramer in plasma membranes of bovine adrenal cortex [J]. J Biochem, 1991, 110(1): 35-9.
[127] LOWE D G. Human natriuretic peptide receptor-A guanylyl cyclase is self-associated prior to hormone binding [J]. Biochemistry, 1992, 31(43): 10421-5.
[128] OGAWA H, QIU Y, OGATA C M, et al. Crystal structure of hormone-bound atrial natriuretic peptide receptor extracellular domain: rotation mechanism for transmembrane signal transduction [J]. J Biol Chem, 2004, 279(27): 28625-31.
[129] LABRECQUE J, MC NICOLL N, MARQUIS M, et al. A disulfide-bridged mutant of natriuretic peptide receptor-A displays constitutive activity. Role of receptor dimerization in signal transduction [J]. J Biol Chem, 1999, 274(14): 9752-9.
[130] CHINKERS M, GARBERS D L. The protein kinase domain of the ANP receptor is required for signaling [J]. Science, 1989, 245(4924): 1392-4.
[131] KOLLER K J, DE SAUVAGE F J, LOWE D G, et al. Conservation of the kinaselike regulatory domain is essential for activation of the natriuretic peptide receptor guanylyl cyclases [J]. Mol Cell Biol, 1992, 12(6): 2581-90.
[132] FOSTER D C, GARBERS D L. Dual role for adenine nucleotides in the regulation of the atrial natriuretic peptide receptor, guanylyl cyclase-A [J]. J Biol Chem, 1998, 273(26): 16311-8.
[133] KUROSE H, 1NAGAMI T, UI M. Participation of adenosine 5'-triphosphate in the activation of membrane-bound guanylate cyclase by the atrial natriuretic factor [J]. FEBS Lett,1987, 219(2): 375-9.
[134] CHINKERS M, SINGH S, GARBERS D L. Adenine nucleotides are required for activation of rat atrial natriuretic peptide receptor/guanylyl cyclase expressed in a baculovirus system [J]. J Biol Chem, 1991, 266(7): 4088-93.
[135] MARALA R B, SITARAMAYYA A, SHARMA R K. Dual regulation of atrial natriuretic factor-dependent guanylate cyclase activity by ATP [J]. FEBS Lett, 1991, 281(1-2): 73-6.
[136] WONG S K, MA C P, FOSTER D C, et al. The guanylyl cyclase-A receptor transduces an atrial natriuretic peptide/ATP activation signal in the absence of other proteins [J]. J Biol Chem, 1995, 270(51): 30818-22.
[137] DUDA T, GORACZNIAK R M, SITARAMAYYA A, et al. Cloning and expression of an ATP-reguIated human retina C-type natriuretic factor receptor guanylate cyclase [J]. Biochemistry,1993,32(6): 1391-5.
[138] ANTOS L K, ABBEY-HOSCH S E, FLORA D R, et al. ATP-independent activation of natriuretic peptide receptors [J]. J Biol Chem, 2005, 280(29): 26928-32.
[139] JEWETT J R, KOLLER K J, GOEDDEL D V, et al. Hormonal induction of low affinity receptor guanylyl cyclase [J]. Embo J, 1993, 12(2): 769-77.
[140] KOH G Y, NUSSENZVEIG D R, OKOLICANY J, et al. Dynamics of atrial natriuretic factor-guanylate cyclase receptors and receptor-ligand complexes in cultured glomerular mesangial and renomedullary interstitial cells [J]. J Biol Chem, 1992, 267(17): 11987-94.
[141] POTTER L R, GARBERS D L. Dephosphorylation of the guanylyl cyclase-A receptor causes desensitization [J]. J Biol Chem, 1992, 267(21): 14531-4.
[142] JOUBERT S, LABRECQUE J, DE LEAN A. Reduced activity of the NPR-A kinase triggers dephosphorylation and homologous desensitization of the receptor [J]. Biochemistry, 2001, 40(37):11096-105.
[143] BRYAN P M, POTTER L R. The atrial natriuretic peptide receptor (NPR-A/GC-A) is dephosphorylated by distinct microcystin-sensitive and magnesium-dependent protein phosphatases [J]. J Biol Chem, 2002, 277(18): 16041-7.
[144] JAUBERT J, JAUBERT F, MARTIN N, et al. Three new allelic mouse mutations that cause skeletal overgrowth involve the natriuretic peptide receptor C gene (Npr3) [J]. Proc Natl Acad Sci U S A, 1999,96(18): 10278-83.
[145] MATSUKAWA N, GRZESIK W J, TAKAHASHI N, et al. The natriuretic peptide clearance receptor locally modulates the physiological effects of the natriuretic peptide system [J]. Proc Natl Acad Sci U S A, 1999, 96(13): 7403-8.
[146] NUSSENZVEIG D R, LEWICKI J A, MAACK T. Cellular mechanisms of the clearance function of type C receptors of atrial natriuretic factor [J]. J Biol Chem, 1990, 265(34): 20952-8.
[147] ANAND-SRIVASTAVA M B, SAIRAM M R, CANTIN M. Ring-deleted analogs of atrial natriuretic factor inhibit adenylate cyclase/cAMP system. Possible coupling of clearance atrial natriuretic factor receptors to adenylate cyclase/cAMP signal transduction system [J]. J Biol Chem,1990, 265(15): 8566-72.
[148] ANAND-SRIVASTAVA M B, SRIVASTAVA A K, CANTIN M. Pertussis toxin attenuates atrial natriuretic factor-mediated inhibition of adenylate cyclase. Involvement of inhibitory guanine nucleotide regulatory protein [J]. J Biol Chem, 1987, 262(11): 4931-4.
[149] BERL T, MANSOUR J, TEITELBAUM I. ANP stimulates phosphoiipase C in cultured RIMCT cells: roles of protein kinases and G protein [J]. Am J Physiol, 1991, 260(4 Pt 2): F590-5.
[150] RESINK T J, SCOTT-BURDEN T, BAUR U, et al. Atrial natriuretic peptide induces breakdown of phosphatidylinositol phosphates in cultured vascular smooth-muscle cells [J]. Eur J Biochem, 1988, 172(2): 499-505.
[151] MURTHY K S, TENG B Q, ZHOU H, et al. G(i-1)/G(i-2)-dependent signaling by single-transmembrane natriuretic peptide clearance receptor [J]. Am J Physiol Gastrointest Liver Physiol, 2000,278(6): G974-80.
[152] POTTER L R. Phosphorylation-dependent regulation of the guanylyl cyclase-linked natriuretic peptide receptor B: dephosphorylation is a mechanism of desensitization [J].Biochemistry, 1998, 37(8): 2422-9.
[153] POTTER L R, HUNTER T. A constitutively "phosphorylated" guanylyl cyclase-linked atrial natriuretic peptide receptor mutant is resistant to desensitization [J]. Mol Biol Cell, 1999, 10(6): 1811-20.
[154] FOWKES R C, FORREST-OWEN W, MCARDLE C A. C-type natriuretic peptide (CNP) effects in anterior pituitary cell lines: evidence for homologous desensitisation of CNP-stimulated cGMP accumulation in alpha T3-1 gonadotroph-derived cells [J]. J Endocrinol, 2000, 166(1): 195-203.
[155] POTTER L R, GARBERS D L. Protein kinase C-dependent desensitization of the atrial natriuretic peptide receptor is mediated by dephosphorylation [J]. J Biol Chem, 1994, 269(20):14636-42.
[156] HANEDA M, KIKKAWA R, MAEDA S, et al. Dual mechanism of angiotensin II inhibits ANP-induced mesangial cGMP accumulation [J]. Kidney Int, 1991,40(2): 188-94.
[157] ABBEY S E, POTTER L R. Vasopressin-dependent inhibition of the C-type natriuretic peptide receptor, NPR-B/GC-B, requires elevated intracellular calcium concentrations [J]. J Biol Chem, 2002, 277(45): 42423-30.
[158] ABBEY S E, POTTER L R. Lysophosphatidic acid inhibits C-type natriuretic peptide activation of guanylyl cyclase-B [J]. Endocrinology, 2003, 144(1): 240-6.
[159] ABBEY-HOSCH S E, CODY A N, POTTER L R. Sphingosine-1-phosphate inhibits C-type natriuretic peptide activation of guanylyl cyclase B (GC-B/NPR-B) [J]. Hypertension, 2004, 43(5):1103-9.
[160] CHR1SMAN T D, PERKINS D T, GARBERS D L. Identification of a potent serum factor that causes desensitization of the receptor for C-Type natriuretic peptide [J]. Cell Commun Signal,2003, 1(1): 4.
[161] CROOK R B, CHANG A T. Differential regulation of natriuretic peptide receptors on ciliary body epithelial cells [J]. Biochem J, 1997, 324 ( Pt 1)(49-55.
[162] JAISWAL R K. Endothelin inhibits the atrial natriuretic factor stimulated cGMP production by activating the protein kinase C in rat aortic smooth muscle cells [J]. Biochem Biophys Res Commun, 1992, 182(1): 395-402.
[163] POTTER L R, HUNTER T. Activation of protein kinase C stimulates the dephosphorylation of natriuretic peptide receptor-B at a single serine residue: a possible mechanism of heterologous desensitization [J]. J Biol Chem, 2000, 275(40): 31099-106.
[164] POTTHAST R, ABBEY-HOSCH S E, ANTOS L K, et al. Calcium-dependent dephosphorylation mediates the hyperosmotic and lysophosphatidic acid-dependent inhibition of natriuretic peptide receptor-B/guanylyl cyclase-B [J]. J Biol Chem, 2004, 279(47): 48513-9.
[165] ABBEY-HOSCH S E, SMIRNOV D, POTTER L R. Differential regulation of NPR-B/GC-B by protein kinase c and calcium [J]. Biochem Pharmacol, 2005, 70(5): 686-94.
[166] CHARLES C J, ESP1NER E A, NICHOLLS M G, et al. Clearance receptors and endopeptidase 24.11: equal role in natriuretic peptide metabolism in conscious sheep [J]. Am J Physiol, 1996, 271(2 Pt 2): R373-80.
[167] SMITH M W, ESP1NER E A, YANDLE T G, et al. Delayed metabolism of human brain natriuretic peptide reflects resistance to neutral endopeptidase [J]. J Endocrinol, 2000, 167(2): 239-46.
[168] ABASSI Z A, TATE J, HUNSBERGER S, et al. Pharmacokinetics of ANF and urodilatin during cANF receptor blockade and neutral endopeptidase inhibition [J]. Am J Physiol, 1992,263(5 Pt1):E870-6.
[169] FAN D, BRYAN P M, ANTOS L K, et al. Down-regulation does not mediate natriuretic peptide-dependent desensitization of natriuretic peptide receptor (NPR)-A or NPR-B: guanylyl cyclase-linked natriuretic peptide receptors do not internalize [J]. Mol Pharmacol, 2005, 67(1):174-83.
[170] MORISH1TA Y, SANO T, ANDO K, et al. Microbial polysaccharide, HS-142-1,competitively and selectively inhibits ANP binding to its guanylyl cyclase-containing receptor [J].Biochem Biophys Res Commun, 1991, 176(3): 949-57.
[171] SANO T, IMURA R, MOR1SH1TA Y, et al. HS-142-1, a novel polysaccharide of microbial origin, specifically recognizes guanylyl cyclase-linked ANP receptor in rat glomeruli [J]. Life Sci,1992,51(18): 1445-51.
[172] POIRIER H, LABRECQUE J, DESCHENES J, et al. Allotopic antagonism of the non-peptide atrial natriuretic peptide (ANP) antagonist HS-142-1 on natriuretic peptide receptor NPR-A [J]. Biochem J, 2002, 362(Pt 1): 231-7.
[173] DELPORTE C, WINAND J, POLOCZEK P, et al. Discovery of a potent atrial natriuretic peptide antagonist for ANPA receptors in the human neuroblastoma NB-OK-1 cell line [J]. Eur J Pharmacol, 1992,224(2-3): 183-8.
[174] VON GELDERN T W, BUDZIK G P, DILLON T P, et al. Atrial natriuretic peptide antagonists: biological evaluation and structural correlations [J]. Mol Pharmacol, 1990, 38(6):771-8.
[175] PANDEY K N. Biology of natriuretic peptides and their receptors [J]. Peptides, 2005, 26(6): 901-32.
[176] CERMAK R, KLETA R, FORSSMANN W G, et al. Natriuretic peptides increase a K+ conductance in rat mesangial cells [J]. Pflugers Arch, 1996, 431(4): 571-7.
[177] KOURIE J I. Calcium dependence of C-type natriuretic peptide-formed fast K(+) channel [J]. Am J Physiol, 1999, 277(1 Pt 1): C43-50.
[178] SANSOM S C, STOCKAND J D, HALL D, et al. Regulation of large calcium-activated potassium channels by protein phosphatase 2A [J]. J Biol Chem, 1997, 272(15): 9902-6.
[179] GUO H S, CAI Z X, ZHENG H F, et al. Role of calcium-activated potassium currents in CNP-induced relaxation of gastric antral circular smooth muscle in guinea pigs [J]. World J Gastroenterol, 2003, 9(9): 2054-9.
[180] BANKS M, WEI C M, KIM C H, et al. Mechanism of relaxations to C-type natriuretic peptide in veins [J]. Am J Physiol, 1996, 271(5 Pt 2): H1907-11.
[181] HIRSCH J R, MEYER M, MAGERT H J, et al. cGMP-dependent and -independent inhibition of a K+ conductance by natriuretic peptides: molecular and functional studies in human proximal tubule cells [J]. J Am Soc Nephrol, 1999, 10(3): 472-80.
[182] DIXON D B, COPENHAGEN D R. Metabotropic glutamate receptor-mediated suppression of an inward rectifier current is linked via a cGMP cascade [J]. J Neurosci, 1997, 17(23): 8945-54.
[183] KANWAL S, ELMQUIST B J, TRACHTE G J. Atrial natriuretic peptide inhibits evoked catecholamine release by altering sensitivity to calcium [J]. J Pharmacol Exp Ther, 1997, 283(2):426-33.
[184] ISALES C M, LEWICKI J A, NEE J J, et al. ANP-(7-23) stimulates a DHP-sensitive Ca2+ conductance and reduces cellular cAMP via a cGMP-independent mechanism [J]. Am J Physiol,1992, 263(2 Pt 1):C334-42.
[185] SINGER I, EPSTEIN M. Potential of dopamine A-1 agonists in the management of acute renal failure [J]. Am J Kidney Dis, 1998, 31(5): 743-55.
[186] GREEN A K, STRATTON R C, SQUIRES P E, et al. Atrial natriuretic peptide attenuates elevations in Ca2+ and protects hepatocytes by stimulating net plasma membrane Ca2+ efflux [J].J Biol Chem, 2007,282(47): 34542-54.
[187] ROSE R A, ANAND-SRIVASTAVA M B, GILES W R, et al. C-type natriuretic peptide inhibits L-type Ca2+ current in rat magnocellular neurosecretory cells by activating the NPR-C receptor [J]. J Neurophysiol, 2005, 94(1): 612-21.
[188] ROSE R A, LOMAX A E, KONDO C S, et al. Effects of C-type natriuretic peptide on ionic currents in mouse sinoatrial node: a role for the NPR-C receptor [J]. Am J Physiol Heart Circ Physiol, 2004, 286(5): H1970-7.
[189] LEE B, LAYCHOCK S G. Atrial natriuretic peptide and cyclic nucleotides affect glucose-induced Ca2+ responses in single pancreatic islet beta-cells: correlation with (Ca[2+] + Mg2+)-ATPase activity [J]. Diabetes, 1997,46(8): 1312-8.
[190] YOSHIZUMI M, HOUCHI H, TSUCHIYA K, et al. Atrial natriuretic peptide stimulates Na+-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes [J]. FEBS Lett, 1997, 419(2-3): 255-8.
[191] FELDER R A, FELDER C C, EISNER G M, et al. The dopamine receptor in adult and maturing kidney [J]. Am J Physiol, 1989, 257(3 Pt 2): F315-27.
[192] KANTOCI D, WECHTER W J, MURRAY E D, JR., et al. Endogenous natriuretic factors 6: the stereochemistry of a natriuretic gamma-tocopherol metabolite LLU-alpha [J]. J Pharmacol Exp Ther, 1997, 282(2): 648-56.
[193] O'BRODOVICH H, RAFII B, PERLON P. Arginine vasopressin and atrial natriuretic peptide do not alter ion transport by cultured fetal distal lung epithelium [J]. Pediatr Res, 1992,31(4 Pt 1): 318-22.
[194] ROSE R A, HATANO N, OHYA S, et al. C-type natriuretic peptide activates a non-selective cation current in acutely isolated rat cardiac fibroblasts via natriuretic peptide C receptor-mediated signalling [J]. J Physiol, 2007, 580(Pt 1): 255-74.
[195] NOVAIRA H J, ORNELLAS D S, ORTIGA-CARVALHO T M, et al. Atrial natriuretic peptide modulates cystic fibrosis transmembrane conductance regulator chloride channel expression in rat proximal colon and human intestinal epithelial cells [J]. J Endocrinol, 2006, 189(1): 155-65.
[196] PIGGOTT L A, HASSELL K A, BERKOVA Z, et al. Natriuretic peptides and nitric oxide stimulate cGMP synthesis in different cellular compartments [J]. J Gen Physiol, 2006, 128(1):3-14.
[1] Todd PA, Sorkin EM. Diclofenac sodium, a reappraisal of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. Drugs 1988; 35: 244-285.
[2] Dawood MY. Nonsteroidal antiinflammatory drugs and reproduction. Am J Obstet Gynecol 1993; 169: 1255-1265.
[3] Small RE. Diclofenac sodium. Clin Pharmacol 1989; 8: 545-558.
[4] Vane JR. Introduction: mechanism of action of NSAIDs. Br J Rheumatol 1996; 35: 1-3.
[5] Tonussi CR, Ferreira SH. Mechanism of diclofenac analgesia: direct blockade of inflammatory sensitization. Euro J Pharmacol 1994; 251: 173-179.
[6] Asomoza-Espinosa R, Alonso-L(?)pez R, Mixcoatl-Zecuatl T, Aguirre-Bafiuelos P, Torres-Lopez JE, Granados-Soto V. Sildenafil increases diclofenac antinociception in the formalin test.Euro J Pharmacol 2001; 418: 195-200.
[7] Alves D, Duarte I. Involvement of ATP-sensitive K~+ channels in the peripheral antinociceptive effect induced by dipyrone. Euro J Pharmacol 2002; 444: 47-52.
[8] Ortiz MI, Torres-Lopez JE, Casta(?)eda-Hem(?)ndez G, Rosas R, Vidal-Cant(?) GC, Granados-Soto V. Pharmacological evidence for the activation of K~+ channels by diclofenac. Euro J Pharmacol 2002; 438: 85-91.
[9] Voilley N, de Weille J, Mamet J, Lazdunski M. Nonsteroid anti-inflammatory drugs inhibit both the activity and the inflammation-induced expression of acid-sensing ion channels in nociceptors. J Neurosci 2001; 21: 8026-8033.
[10] Lee HM, Kim HI, Shin YK, Lee CS, Park M, Song JH. Diclofenac inhibition of sodium currents in rat dorsal root ganglion neurons. Brain Res 2003; 992: 120-127.
[11] Liu LY, Hu CL, Ma LJ, Zhang ZH, Mei YA. ET-1 inhibits B-16 murine melanoma cell migration by decreasing K~+ currents. Cell Motil Cytoskeleton 2004; 58: 127-136.
[12] Liu LY, Fei XW, Li ZM, Zhang ZH, Mei YA. Diclofenac, a nonsteroidal anti-inflammatory drug, activates the transient outward K~+ current in rat cerebellar granule cells.Neuropharmacology 2005; 48: 918-926.
[13] Occhiodoro T, Bernheim L, Liu JH, Bijlenga P, Sinnreich M, Bader CR, et al. Cloning of a human ether-a-go-go potassium channel expressed in myoblasts at the onset of fusion. FEBS Lett 1998; 434: 177-182.
[14] Bijlenga P, Liu JH, Espinos E, Haenggeli CA, Fischer-Lougheed J, Bader CR, et al. T-type alH Ca~(2+) channels are involved in Ca~(2+) signaling during terminalH Ca~(2+) channels are involved in Ca~(2+) signaling during terminal differentiation (fusion) of human myoblasts. Proc Natl Acad Sci USA 2000; 97: 7627-7632.
[15] Fischer-Lougheed J, Liu JH, Espinos E, Mordasini D, Bader CR, Belin D, et al. Human myoblast fusion requires expression of functional inward rectifier Kir2.1 channels. J Cell Biol 2001; 153: 677-685.
[16] Zhou MO, Liu Z, Hu CL, Zhang ZH, Mei YA. Developmental Regulation of a Na~+-activated Fast Outward K~+ Current in Rat Myoblasts. Cell Physiol Biochem 2004; 14: 225-230.
[17] Lu BX, Liu LY, Liao L, Zhang ZH, Mei YA. Inhibition of Na~+ channel currents in rat myoblasts by 4-aminopyridine. Toxicol Appl Pharm 2005; 207: 275-282.
[18] Kuo CC, Huang RC, Lou BS. Inhibition of Na~+ current by diphenhydramine and other diphenyl compounds: molecular determinants of selective binding to the inactivated channels.Mol Pharmacol 2000; 57: 135-143.
[19] Yang YC, Kuo CC. An Inactivation Stabilizer of the Na~+ Channel Acts as an Opportunistic Pore Blocker Modulated by External Na~+. J Gen Physiol 2005; 125: 465-481.
[20] Fozzard HA, Hanck DA. Structure and function of voltage-dependent sodium channels: comparison of brainⅡ and cardiac isoforms. Physiol Rev 1996; 76: 887-926.
[21] Catterall WA. From ionic current to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron 2000; 26: 13-25.
[22] Nuss HB, Tomaselli GF, Marban E. Cardiac sodium channels (hH1) are intrinsically more sensitive to block by lidocaine than are skeletal muscle (μ1) channels. J Gen Physiol 1995; 106:1193-1209.
[23] Li RA, Ennis IL, Tomaselli GF, Marban E. Structural basis of differences in isoform-specific gating and lidocaine blocking between cardiac and skeletal muscle sodium channels. Mol Pharmacol 2002; 61: 136-141.
[24] Goldin AL. Resurgence of sodium channel research. Annu Rev Physiol 2001; 63: 871-894.
[25] Goldin AL. Diversity of Mammalian Voltage-Gated Sodium Channels. Ann NY Acad Sci 1999; 868:38-50.
[26] Butterworth JF, Strichartz GR. Molecular mechanisms of local anesthesia: a review. Anesthesiology 1990; 72: 711-734.
[27] Laerum E, Ommundsen OE, Gronseth JE, Christiansen A, Fagertun HE. Oral diclofenac in the prophylactic treatment of recurrent renal colic. A double-blind comparison with placebo.Eur Urol 1995; 28: 108-111.
[28] Laerum E, Murtagh J. Renal colic and recurrent urinary calculi. Management and prevention. Aust Fam Physician 2001; 30: 36-41.
[29] Jett MF, Ramesha CS, Brown CD, Chiu S, Emmett C, Voronin T, et al. Characterization of the analgesic and anti-inflammatory activities of ketorolac and its enantiomers in the rat. J Pharmacol Exp Therap 1999; 288: 1288-1297.
[2] SUDOH T, KANGAWA K, MINAMINO N, et al. A new natriuretic peptide in porcine brain [J]. Nature, 1988, 332(6159): 78-81.
[3] SUDOH T, MINAMINO N, KANGAWA K, et al. C-type natriuretic peptide (CNP): a new member of natriuretic peptide family identified in porcine brain [J]. Biochem Biophys Res Commun, 1990, 168(2): 863-70.
[4] DICICCO-BLOOM E, LELIEVRE V, ZHOU X, et al. Embryonic expression and multifunctional actions of the natriuretic peptides and receptors in the developing nervous system [J]. Dev Biol, 2004, 271(1): 161-75.
[5] INOHA S, INAMURA T, NAKAMIZO A, et al. Fluid loading in rats increases serum brain natriuretic peptide concentration [J]. Neurol Res, 2001, 23(1): 93-5.
[6] DE BOLD A J, DE BOLD M L. Determinants of natriuretic peptide production by the heart: basic and clinical implications [J]. J Investig Med, 2005, 53(7): 371-7.
[7] SVIRI G E, SHIK V, RAZ B, et al. Role of brain natriuretic peptide in cerebral vasospasm [J]. Acta Neurochir(Wien), 2003, 145(10): 851-60; discussion 60.
[8] BIGGIN P C, ROOSILD T, CHOE S. Potassium channel structure: domain by domain [J]. Curr Opin Struct Biol, 2000, 10(4): 456-61.
[9] DAI S, HALL D D, HELL J W. Supramolecular assemblies and localized regulation of voltage-gated ion channels [J]. Physiol Rev, 2009, 89(2): 411-52.
[10] Molecular and Functional Diversity of Ion Channels and Receptors. Proceedings of a conference. New York City, New York, USA. May 14-17, 1998 [J]. Ann N Y Acad Sci, 1999,868(1-774.
[11] RETTIG J, HEINEMANN S H, WUNDER F, et al. Inactivation properties of voltage-gated K+ channels altered by presence of beta-subunit [J]. Nature, 1994, 369(6478): 289-94.
[12] SHI G, NAKAHIRA K, HAMMOND S, et al. Beta subunits promote K+ channel surface expression through effects early in biosynthesis [J]. Neuron, 1996, 16(4): 843-52.
[13] NAGAYA N, PAPAZIAN D M. Potassium channel alpha and beta subunits assemble in the endoplasmic reticulum [J]. J Biol Chem, 1997, 272(5): 3022-7.
[14] YU Y C, CAO L H, YANG X L. Modulation by brain natriuretic peptide of GABA receptors on rat retinal ON-type bipolar cells [J]. J Neurosci, 2006, 26(2): 696-707.
[15] XU H Y, HUANG X, YANG M, et al. The effect of C-type natriuretic peptide on delayed rectifier potassium currents in gastric antral circular myocytes of the guinea-pig [J]. Physiol Res,2008, 57(1): 55-62.
[16] TANAKA Y, TANG G, TAKIZAWA K, et al. Kv channels contribute to nitric oxide- and atrial natriuretic peptide-induced relaxation of a rat conduit artery [J]. J Pharmacol Exp Ther, 2006,317(1):341-54.
[17] FAGNI L, BOSSU J L, BOCKAERT J. Activation of a Large-conductance Ca2+-Dependent K+ Channel by Stimulation of Glutamate Phosphoinositide-coupled Receptors in Cultured Cerebellar Granule Cells [J]. Eur J Neurosci, 1991, 3(8): 778-89.
[18] WATKINS C S, MATHIE A. Modulation of the gating of the transient outward potassium current of rat isolated cerebellar granule neurons by lanthanum [J]. Pflugers Arch, 1994, 428(3-4): 209-16.
[19] WATKINS C S, MATHIE A. A non-inactivating K+ current sensitive to muscarinic receptor activation in rat cultured cerebellar granule neurons [J]. J Physiol, 1996,491 (Pt 2)(401-12.
[20] HU C L, LIU Z, GAO Z Y, et al. 2-iodomelatonin prevents apoptosis of cerebellar granule neurons via inhibition of A-type transient outward K+ currents [J]. J Pineal Res, 2005, 38(1):53-61.
[21] JIAO S, WU M M, HU C L, et al. Melatonin receptor agonist 2-iodomelatonin prevents apoptosis of cerebellar granule neurons via K(+) current inhibition [J]. J Pineal Res, 2004, 36(2):109-16.
[22] LIU L Y, HOFFMAN G E, FEI X W, et al. Delayed rectifier outward K+ current mediates the migration of rat cerebellar granule cells stimulated by melatonin [J]. J Neurochem, 2007, 102(2):333-44.
[23] VACHER H, MOHAPATRA D P, TRIMMER J S. Localization and targeting of voltage-dependent ion channels in mammalian central neurons [J]. Physiol Rev, 2008, 88(4):1407-47.
[24] FROSTICK S P, YIN Q, KEMP G J. Schwann cells, neurotrophic factors, and peripheral nerve regeneration [J]. Microsurgery, 1998, 18(7): 397-405.
[25] BAKER M D. Electrophysiology of mammalian Schwann cells [J]. Prog Biophys Mol Biol, 2002, 78(2-3): 83-103.
[26] SOBKO A, PERETZ A, SHIR1HAI O, et al. Heteromultimeric delayed-rectifier K+ channels in schwann cells: developmental expression and role in cell proliferation [J]. J Neurosci, 1998, 18(24): 10398-408.
[27] MI H, DEERINCK T J, ELLISMAN M H, et al. Differential distribution of closely related potassium channels in rat Schwann cells [J]. J Neurosci, 1995, 15(5 Pt 2): 3761-74.
[28] WILSON G F, CHIU S Y. Potassium channel regulation in Schwann cells during early developmental myelinogenesis [J]. J Neurosci, 1990, 10(5): 1615-25.
[29] PERETZ A, SOBKO A, ATTALI B. Tyrosine kinases modulate K+ channel gating in mouse Schwann cells [J]. J Physiol, 1999, 519 Pt 2(373-84.
[30] ROOTS B I. Comparative studies on glial markers [J]. J Exp Biol, 1981, 95(167-80.
[31] YUAN C, YANG S, LIAO Z, et al. Effects and mechanism of Chinese tarantula toxins on the Kv2.1 potassium channels [J]. Biochem Biophys Res Commun, 2007, 352(3): 799-804.
[32] HIRSCH J, SCHLATTER E. Genistein potentiates the ANP effect on a K(+)-conductance in HEK-293 cells [J]. Cell Physiol Biochem, 2003, 13(4): 223-8.
[33] AIRHART N, YANG Y F, ROBERTS C T, JR., et al. Atrial natriuretic peptide induces natriuretic peptide receptor-cGMP-dependent protein kinase interaction [J]. J Biol Chem, 2003,278(40): 38693-8.
[34] NITABACH M N, LLAMAS D A, THOMPSON I J, et al. Phosphorylation-dependent and phosphorylation-independent modes of modulation of shaker family voltage-gated potassium channels by SRC family protein tyrosine kinases [J]. J Neurosci, 2002, 22(18): 7913-22.
[35] SOBKO A, PERETZ A, ATTALI B. Constitutive activation of delayed-rectifier potassium channels by a src family tyrosine kinase in Schwann cells [J]. Embo J, 1998, 17(16): 4723-34.
[36] LELIEVRE V, PINEAU N, HU Z, et al. Proliferative actions of natriuretic peptides on neuroblastoma cells. Involvement of guanylyl cyclase and non-guanylyl cyclase pathways [J]. J Biol Chem, 2001, 276(47): 43668-76.
[37] DE BOLD A J. Atrial natriuretic factor: a hormone produced by the heart [J]. Science, 1985, 230(4727): 767-70.
[38] NAPIER M A, DEWEY R S, ALBERS-SCHONBERG G, et al. Isolation and sequence determination of peptide components of atrial natriuretic factor [J]. Biochem Biophys Res Commun, 1984, 120(3): 981-8.
[39] MISONO K S, GRAMMER R T, FUKUMI H, et al. Rat atrial natriuretic factor: isolation, structure and biological activities of four major peptides [J]. Biochem Biophys Res Commun,1984, 123(2): 444-51.
[40] FLYNN T G, DE BOLD M L, DE BOLD A J. The amino acid sequence of an atrial peptide with potent diuretic and natriuretic properties [J]. Biochem Biophys Res Commun, 1983, 117(3):859-65.
[41] CURRIE M G, GELLER D M, COLE B R, et al. Purification and sequence analysis of bioactive atrial peptides (atriopeptins) [J]. Science, 1984, 223(4631): 67-9.
[42] KANGAWA K, TAWARAGI Y, OIKAWA S, et al. Identification of rat gamma atrial natriuretic polypeptide and characterization of the cDNA encoding its precursor [J]. Nature, 1984,312(5990): 152-5.
[43] MCGRATH M F, DE BOLD A J. Determinants of natriuretic peptide gene expression [J]. Peptides, 2005, 26(6): 933-43.
[44] TAKEI Y. Structural and functional evolution of the natriuretic peptide system in vertebrates [J]. Int Rev Cytol, 2000, 194(1-66.
[45] INOUE K, NARUSE K, YAMAGAMI S, et al. Four functionally distinct C-type natriuretic peptides found in fish reveal evolutionary history of the natriuretic peptide system [J]. Proc Natl Acad Sci U S A, 2003, 100(17): 10079-84.
[46] GUTKOWSKA J, NEMER M. Structure, expression, and function of atrial natriuretic factor in extraatrial tissues [J]. Endocr Rev, 1989, 10(4): 519-36.
[47] GU J, D'ANDREA M, SEETHAPATHY M. Atrial natriuretic peptide and its messenger ribonucleic acid in overloaded and overload-released ventricles of rat [J]. Endocrinology, 1989,125(4): 2066-74.
[48] SA1TO Y, NAKAO K, ARAI H, et al. Augmented expression of atrial natriuretic polypeptide gene in ventricle of human failing heart [J]. J Clin Invest, 1989, 83(1): 298-305.
[49] STASCH J P, HIRTH-DIETRICH C, KAZDA S, et al. Endothelin stimulates release of atrial natriuretic peptides in vitro and in vivo [J]. Life Sci, 1989, 45(10): 869-75.
[50] SOUALMIA H, BARTHELEMY C, MASSON F, et al. Angiotensin Ⅱ-induced phosphoinositide production and atrial natriuretic peptide release in rat atrial tissue [J]. J Cardiovasc Pharmacol, 1997, 29(5): 605-11.
[51] LACHANCE D, GARCIA R, GUTKOWSKA J, et al. Mechanisms of release of atrial natriuretic factor. I. Effect of several agonists and steroids on its release by atrial minces [J].Biochem Biophys Res Commun, 1986, 135(3): 1090-8.
[52] THIBAULT G, AMIRI F, GARCIA R. Regulation of natriuretic peptide secretion by the heart [J]. Annu Rev Physiol, 1999, 61(193-217.
[53] EDWARDS B S, ZIMMERMAN R S, SCHWAB T R, et al. Atrial stretch, not pressure, is the principal determinant controlling the acute release of atrial natriuretic factor [J]. Circ Res, 1988, 62(2): 191-5.
[54] CODY R J, ATLAS S A, LARAGH J H, et al. Atrial natriuretic factor in normal subjects and heart failure patients. Plasma levels and renal, hormonal, and hemodynamic responses to peptide infusion [J]. J Clin Invest, 1986, 78(5): 1362-74.
[55] YANG-FENG T L, FLOYD-SMITH G, NEMER M, et al. The pronatriodilatin gene is located on the distal short arm of human chromosome 1 and on mouse chromosome 4 [J]. Am J Hum Genet, 1985, 37(6): 1117-28.
[56] MAKI M, TAKAYANAGI R, MISONO K S, et al. Structure of rat atrial natriuretic factor precursor deduced from cDNA sequence [J]. Nature, 1984, 309(5970): 722-4.
[57] YAMANAKA M, GREENBERG B, JOHNSON L, et al. Cloning and sequence analysis of the cDNA for the rat atrial natriuretic factor precursor [J]. Nature, 1984, 309(5970): 719-22.
[58] YAN W, WU F, MORSER J, et al. Corin, a transmembrane cardiac serine protease, acts as a pro-atrial natriuretic peptide-converting enzyme [J]. Proc Natl Acad Sci U S A, 2000, 97(15):8525-9.
[59] CHAN J C, KNUDSON O, WU F, et al. Hypertension in mice lacking the proatrial natriuretic peptide convertase corin [J]. Proc Natl Acad Sci U S A, 2005, 102(3): 785-90.
[60] WU F, YAN W, PAN J, et al. Processing of pro-atrial natriuretic peptide by corin in cardiac myocytes [J]. J Biol Chem, 2002, 277(19): 16900-5.
[61] GARDNER D G, CHEN S, GLENN D J, et al. Molecular biology of the natriuretic peptide system: implications for physiology and hypertension [J]. Hypertension, 2007, 49(3): 419-26.
[62] SCHULZ-KNAPPE P, FORSSMANN K, HERBST F, et al. Isolation and structural analysis of "urodilatin", a new peptide of the cardiodilatin-(ANP)-family, extracted from human urine [J].Klin Wochenschr, 1988, 66(17): 752-9.
[63] FORSSMANN W G, RICHTER R, MEYER M. The endocrine heart and natriuretic peptides: histochemistry, cell biology, and functional aspects of the renal urodilatin system [J]. Histochem Cell Biol, 1998, 110(4): 335-57.
[64] MUKOYAMA M, NAKAO K, HOSODA K, et al. Brain natriuretic peptide as a novel cardiac hormone in humans. Evidence for an exquisite dual natriuretic peptide system, atrial natriuretic peptide and brain natriuretic peptide [J]. J Clin Invest, 1991, 87(4): 1402-12.
[65] GREPIN C, DAGN1NO L, ROBITAILLE L, et al. A hormone-encoding gene identifies a pathway for cardiac but not skeletal muscle gene transcription [J]. Mol Cell Biol, 1994, 14(5): 3115-29.
[66] THUERAUF D J, HANFORD D S, GLEMBOTSKI C C. Regulation of rat brain natriuretic peptide transcription. A potential role for G ATA-related transcription factors in myocardial cell gene expression [J]. J Biol Chem, 1994, 269(27): 17772-5.
[67] TOGASHI K, ANDO K, HASEGAWA N, et al. Concentrations of brain natriuretic peptide in treated congestive heart failure [J]. Clin Chem, 1991, 37(5): 765.
[68] TAMURA N, OGAWA Y, CHUSHO H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide [J]. Proc Natl Acad Sci U S A, 2000,97(8): 4239-44.
[69] SEILHAMER J J, ARFSTEN A, MILLER J A, et al. Human and canine gene homologs of porcine brain natriuretic peptide [J]. Biochem Biophys Res Commun, 1989, 165(2): 650-8.
[70] SUDOH T, MINAMINO N, KANGAWA K, et al. Brain natriuretic peptide-32: N-terminal six amino acid extended form of brain natriuretic peptide identified in porcine brain [J]. Biochem Biophys Res Commun, 1988, 155(2): 726-32.
[71] OGAWA Y, ITOH H, TAMURA N, et al. Molecular cloning of the complementary DNA and gene that encode mouse brain natriuretic peptide and generation of transgenic mice that overexpress the brain natriuretic peptide gene [J]. J Clin Invest, 1994, 93(5): 1911-21.
[72] KOJIMA M, MINAMINO N, KANGAWA K, et al. Cloning and sequence analysis of cDNA encoding a precursor for rat brain natriuretic peptide [J]. Biochem Biophys Res Commun, 1989, 159(3): 1420-6.
[73] SUDOH T, MAEKAWA K, KOJIMA M, et al. Cloning and sequence analysis of cDNA encoding a precursor for human brain natriuretic peptide [J]. Biochem Biophys Res Commun,1989, 159(3): 1427-34.
[74] HAGIWARA H, SAKAGUCHI H, ITAKURA M, et al. Autocrine regulation of rat chondrocyte proliferation by natriuretic peptide C and its receptor, natriuretic peptide receptor-B [J]. J Biol Chem, 1994, 269(14): 10729-33.
[75] HAGIWARA H, SAKAGUCHI H, LODHI K M, et al. Subtype switching of natriuretic peptide receptors in rat chondrocytes during in vitro culture [J]. J Biochem, 1994, 116(3): 606-9.
[76] SUGA S, NAKAO K, ITOH H, et al. Endothelial production of C-type natriuretic peptide and its marked augmentation by transforming growth factor-beta. Possible existence of "vascular natriuretic peptide system" [J]. J Clin Invest, 1992, 90(3): 1145-9.
[77] SUGA S, ITOH H, KOMATSU Y, et al. Cytokine-induced C-type natriuretic peptide (CNP) secretion from vascular endothelial cells-evidence for CNP as a novel autocrine/paracrine regulator from endothelial cells [J]. Endocrinology, 1993, 133(6): 3038-41.
[78] IGAKI T, ITOH H, SUGA S, et al. Insulin suppresses endothelial secretion of C-type natriuretic peptide, a novel endothelium-derived relaxing peptide [J]. Diabetes, 1996, 45 Suppl 3(S62-4.
[79] KALRA P R, CLAGUE J R, BOLGER A P, et al. Myocardial production of C-type natriuretic peptide in chronic heart failure [J]. Circulation, 2003, 107(4): 571-3.
[80] WEI C M, HEUBLEIN D M, PERRELLA M A, et al. Natriuretic peptide system in human heart failure [J]. Circulation, 1993, 88(3): 1004-9.
[81] CHUSHO H, TAMURA N, OGAWA Y, et al. Dwarfism and early death in mice lacking C-type natriuretic peptide [J]. Proc Natl Acad Sci U S A, 2001, 98(7): 4016-21.
[82] NAKAYAMA T. The genetic contribution of the natriuretic peptide system to cardiovascular diseases [J]. Endocr J, 2005, 52(1): 11-21.
[83] OGAWA Y, ITOH H, YOSHITAKE Y, et al. Molecular cloning and chromosomal assignment of the mouse C-type natriuretic peptide (CNP) gene (Nppc): comparison with the human CNP gene (NPPC) [J]. Genomics, 1994, 24(2): 383-7.
[84] OGAWA Y, NAKAO K, NAKAGAWA O, et al. Human C-type natriuretic peptide. Characterization of the gene and peptide [J]. Hypertension, 1992, 19(6 Pt 2): 809-13.
[85] WU C, WU F, PAN J, et al. Furin-mediated processing of Pro-C-type natriuretic peptide [J]. J Biol Chem, 2003, 278(28): 25847-52.
[86] YEUNG V T, HO S K, NICHOLLS M G, et al. Binding of CNP-22 and CNP-53 to cultured mouse astrocytes and effects on cyclic GMP [J]. Peptides, 1996, 17(1): 101-6.
[87] TAWARAGI Y, FUCH1MURA K, TANAKA S, et al. Gene and precursor structures of human C-type natriuretic peptide [J]. Biochem Biophys Res Commun, 1991, 175(2): 645-51.
[88] TOTSUNE K, TAKAHASHI K, OHNEDA M, et al. C-type natriuretic peptide in the human central nervous system: distribution and molecular form [J]. Peptides, 1994, 15(1): 37-40.
[89] STINGO A J, CLAVELL A L, HEUBLEIN D M, et al. Presence of C-type natriuretic peptide in cultured human endothelial cells and plasma [J]. Am J Physiol, 1992, 263(4 Pt 2): H1318-21.
[90] MINAMINO N, MAKINO Y, TATEYAMA H, et al. Characterization of immunoreactive human C-type natriuretic peptide in brain and heart [J]. Biochem Biophys Res Commun, 1991,179(1): 535-42.
[91] TOGASHI K, KAMEYA T, KUROSAWA T, et al. Concentrations and molecular forms of C-type natriuretic peptide in brain and cerebrospinal fluid [J]. Clin Chem, 1992, 38(10): 2136-9.
[92] GREENBERG R N, HILL M, CRYTZER J, et al. Comparison of effects of uroguanylin, guanylin, and Escherichia coli heat-stable enterotoxin STa in mouse intestine and kidney:evidence that uroguanylin is an intestinal natriuretic hormone [J]. J Investig Med, 1997, 45(5): 276-82.
[93] SCHWEITZ H, VIGNE P, MOINIER D, et al. A new member of the natriuretic peptide family is present in the venom of the green mamba (Dendroaspis angusticeps) [J]. J Biol Chem, 1992, 267(20): 13928-32.
[94] LISY O, JOUGASAKI M, HEUBLEIN D M, et al. Renal actions of synthetic dendroaspis natriuretic peptide [J]. Kidney Int, 1999, 56(2): 502-8.
[95] THOMAS G, MOFFATT P, SALOIS P, et al. Osteocrin, a novel bone-specific secreted protein that modulates the osteoblast phenotype [J]. J Biol Chem, 2003,278(50): 50563-71.
[96] NISHIZAWA H, MATSUDA M, YAMADA Y, et al. Musclin, a novel skeletal muscle-derived secretory factor [J]. J Biol Chem, 2004, 279(19): 19391-5.
[97] MOFFATT P, THOMAS G, SELLIN K, et al. Osteocrin is a specific ligand of the natriuretic Peptide clearance receptor that modulates bone growth [J]. J Biol Chem, 2007, 282(50): 36454-62.
[98] LOWE D G, CHANG M S, HELLMISS R, et al. Human atrial natriuretic peptide receptor defines a new paradigm for second messenger signal transduction [J]. Embo J, 1989, 8(5):1377-84.
[99] SCHULZ S, SINGH S, BELLET R A, et al. The primary structure of a plasma membrane guanylate cyclase demonstrates diversity within this new receptor family [J]. Cell, 1989, 58(6):1155-62.
[100] NAGASE M, KATAFUCHI T, HIROSE S, et al. Tissue distribution and localization of natriuretic peptide receptor subtypes in stroke-prone spontaneously hypertensive rats [J]. J Hypertens, 1997, 15(11): 1235-43.
[101] WILCOX J N, AUGUSTINE A, GOEDDEL D V, et al. Differential regional expression of three natriuretic peptide receptor genes within primate tissues [J]. Mol Cell Biol, 1991, 11(7):3454-62.
[102] HERMAN J P, DOLGAS C M, RUCKER D, et al. Localization of natriuretic peptide-activated guanylate cyclase mRNAs in the rat brain [J]. J Comp Neurol, 1996, 369(2): 165-87.
[103] LANGUB M C, JR., DOLGAS C M, WATSON R E, JR., et al. The C-type natriuretic peptide receptor is the predominant natriuretic peptide receptor mRNA expressed in rat hypothalamus [J]. J Neuroendocrinol, 1995,7(4): 305-9.
[104] POTTER L R, HUNTER T. Phosphorylation of the kinase homology domain is essential for activation of the A-type natriuretic peptide receptor [J]. Mol Cell Biol, 1998, 18(4): 2164-72.
[105] FETHIERE J, GRAIHLE R, LAROSE L, et al. Distribution and regulation of natriuretic factor-RlC receptor subtypes in mammalian cell lines [J]. Mol Cell Biochem, 1993, 124(1): 11-6.
[106] POTTER L R, HUNTER T. Guanylyl cyclase-linked natriuretic peptide receptors: structure and regulation [J]. J Biol Chem, 2001, 276(9): 6057-60.
[107] POTTER L R. Domain analysis of human transmembrane guanylyl cyclase receptors: implications for regulation [J]. Front Biosci, 2005, 10(1205-20.
[108] SUGA S, NAKAO K, HOSODA K, et al. Receptor selectivity of natriuretic peptide family, atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide [J].Endocrinology, 1992, 130(1): 229-39.
[109] TAKAHASHI Y, NAKAYAMA T, SOMA M, et al. Organization of the human natriuretic peptide receptor A gene [J]. Biochem Biophys Res Commun, 1998, 246(3): 736-9.
[110] YAMAGUCH1 M, RUTLEDGE L J, GARBERS D L. The primary structure of the rat guanylyl cyclase A/atrial natriuretic peptide receptor gene [J]. J Biol Chem, 1990, 265(33):20414-20.
[111] LOPEZ M J, WONG S K, K1SHIMOTO I, et al. Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide [J]. Nature, 1995, 378(6552):65-8.
[112] OLIVER P M, FOX J E, KIM R, et al. Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A [J]. Proc Natl Acad Sci U S A, 1997, 94(26):14730-5.
[113] CHRISMAN T D, SCHULZ S, POTTER L R, et al. Seminal plasma factors that cause large elevations in cellular cyclic GMP are C-type natriuretic peptides [J]. J Biol Chem, 1993, 268(5): 3698-703.
[114] KOLLER K J, GOEDDEL D V. Molecular biology of the natriuretic peptides and their receptors [J]. Circulation, 1992, 86(4): 1081-8.
[115] REHEMUDULA D, NAKAYAMA T, SOMA M, et al. Structure of the type B human natriuretic peptide receptor gene and association of a novel microsatellite polymorphism with essential hypertension [J]. Circ Res, 1999, 84(5): 605-10.
[116] BARTELS C F, BUKULMEZ H, PADAYATTI P, et al. Mutations in the transmembrane natriuretic peptide receptor NPR-B impair skeletal growth and cause acromesomelic dysplasia, type Maroteaux [J]. Am J Hum Genet, 2004, 75(1): 27-34.
[117] PORTER J G, ARFSTEN A, FULLER F, et al. Isolation and functional expression of the human atrial natriuretic peptide clearance receptor cDNA [J]. Biochem Biophys Res Commun,1990, 171(2): 796-803.
[118] VAN DEN AKKER F. Structural insights into the ligand binding domains of membrane bound guanylyl cyclases and natriuretic peptide receptors [J]. J Mol Biol, 2001, 311(5): 923-37.
[119] FULLER F, PORTER J G, ARFSTEN A E, et al. Atrial natriuretic peptide clearance receptor. Complete sequence and functional expression of cDNA clones [J]. J Biol Chem, 1988, 263(19):9395-401.
[120] STULTS J T, O'CONNELL K L, GARCIA C, et al. The disulfide linkages and glycosylation sites of the human natriuretic peptide receptor-C homodimer [J]. Biochemistry, 1994, 33(37):11372-81.
[121] ITAKURA M, IWASHINA M, MIZUNO T, et al. Mutational analysis of disulfide bridges in the type C atrial natriuretic peptide receptor [J]. J Biol Chem, 1994, 269(11): 8314-8.
[122] MAACK T, SUZUKI M, ALMEIDA F A, et al. Physiological role of silent receptors of atrial natriuretic factor [J]. Science, 1987, 238(4827): 675-8.
[123] HE X L, DUKKIPATI A, WANG X, et al. A new paradigm for hormone recognition and allosteric receptor activation revealed from structural studies of NPR-C [J]. Peptides, 2005, 26(6):1035-43.
[124] RAHMUTULA D, NAKAYAMA T, SOMA M, et al. Structure and polymorphisms of the human natriuretic peptide receptor C gene [J]. Endocrine, 2002, 17(2): 85-90.
[125] CHINKERS M, WILSON E M. Ligand-independent oligomerization of natriuretic peptide receptors. Identification of heteromeric receptors and a dominant negative mutant [J]. J Biol Chem,1992,267(26): 18589-97.
[126] IWATA T, UCHIDA-MIZUNO K, KATAFUCHI T, et al. Bifunctional atrial natriuretic peptide receptor (type A) exists as a disulfide-linked tetramer in plasma membranes of bovine adrenal cortex [J]. J Biochem, 1991, 110(1): 35-9.
[127] LOWE D G. Human natriuretic peptide receptor-A guanylyl cyclase is self-associated prior to hormone binding [J]. Biochemistry, 1992, 31(43): 10421-5.
[128] OGAWA H, QIU Y, OGATA C M, et al. Crystal structure of hormone-bound atrial natriuretic peptide receptor extracellular domain: rotation mechanism for transmembrane signal transduction [J]. J Biol Chem, 2004, 279(27): 28625-31.
[129] LABRECQUE J, MC NICOLL N, MARQUIS M, et al. A disulfide-bridged mutant of natriuretic peptide receptor-A displays constitutive activity. Role of receptor dimerization in signal transduction [J]. J Biol Chem, 1999, 274(14): 9752-9.
[130] CHINKERS M, GARBERS D L. The protein kinase domain of the ANP receptor is required for signaling [J]. Science, 1989, 245(4924): 1392-4.
[131] KOLLER K J, DE SAUVAGE F J, LOWE D G, et al. Conservation of the kinaselike regulatory domain is essential for activation of the natriuretic peptide receptor guanylyl cyclases [J]. Mol Cell Biol, 1992, 12(6): 2581-90.
[132] FOSTER D C, GARBERS D L. Dual role for adenine nucleotides in the regulation of the atrial natriuretic peptide receptor, guanylyl cyclase-A [J]. J Biol Chem, 1998, 273(26): 16311-8.
[133] KUROSE H, 1NAGAMI T, UI M. Participation of adenosine 5'-triphosphate in the activation of membrane-bound guanylate cyclase by the atrial natriuretic factor [J]. FEBS Lett,1987, 219(2): 375-9.
[134] CHINKERS M, SINGH S, GARBERS D L. Adenine nucleotides are required for activation of rat atrial natriuretic peptide receptor/guanylyl cyclase expressed in a baculovirus system [J]. J Biol Chem, 1991, 266(7): 4088-93.
[135] MARALA R B, SITARAMAYYA A, SHARMA R K. Dual regulation of atrial natriuretic factor-dependent guanylate cyclase activity by ATP [J]. FEBS Lett, 1991, 281(1-2): 73-6.
[136] WONG S K, MA C P, FOSTER D C, et al. The guanylyl cyclase-A receptor transduces an atrial natriuretic peptide/ATP activation signal in the absence of other proteins [J]. J Biol Chem, 1995, 270(51): 30818-22.
[137] DUDA T, GORACZNIAK R M, SITARAMAYYA A, et al. Cloning and expression of an ATP-reguIated human retina C-type natriuretic factor receptor guanylate cyclase [J]. Biochemistry,1993,32(6): 1391-5.
[138] ANTOS L K, ABBEY-HOSCH S E, FLORA D R, et al. ATP-independent activation of natriuretic peptide receptors [J]. J Biol Chem, 2005, 280(29): 26928-32.
[139] JEWETT J R, KOLLER K J, GOEDDEL D V, et al. Hormonal induction of low affinity receptor guanylyl cyclase [J]. Embo J, 1993, 12(2): 769-77.
[140] KOH G Y, NUSSENZVEIG D R, OKOLICANY J, et al. Dynamics of atrial natriuretic factor-guanylate cyclase receptors and receptor-ligand complexes in cultured glomerular mesangial and renomedullary interstitial cells [J]. J Biol Chem, 1992, 267(17): 11987-94.
[141] POTTER L R, GARBERS D L. Dephosphorylation of the guanylyl cyclase-A receptor causes desensitization [J]. J Biol Chem, 1992, 267(21): 14531-4.
[142] JOUBERT S, LABRECQUE J, DE LEAN A. Reduced activity of the NPR-A kinase triggers dephosphorylation and homologous desensitization of the receptor [J]. Biochemistry, 2001, 40(37):11096-105.
[143] BRYAN P M, POTTER L R. The atrial natriuretic peptide receptor (NPR-A/GC-A) is dephosphorylated by distinct microcystin-sensitive and magnesium-dependent protein phosphatases [J]. J Biol Chem, 2002, 277(18): 16041-7.
[144] JAUBERT J, JAUBERT F, MARTIN N, et al. Three new allelic mouse mutations that cause skeletal overgrowth involve the natriuretic peptide receptor C gene (Npr3) [J]. Proc Natl Acad Sci U S A, 1999,96(18): 10278-83.
[145] MATSUKAWA N, GRZESIK W J, TAKAHASHI N, et al. The natriuretic peptide clearance receptor locally modulates the physiological effects of the natriuretic peptide system [J]. Proc Natl Acad Sci U S A, 1999, 96(13): 7403-8.
[146] NUSSENZVEIG D R, LEWICKI J A, MAACK T. Cellular mechanisms of the clearance function of type C receptors of atrial natriuretic factor [J]. J Biol Chem, 1990, 265(34): 20952-8.
[147] ANAND-SRIVASTAVA M B, SAIRAM M R, CANTIN M. Ring-deleted analogs of atrial natriuretic factor inhibit adenylate cyclase/cAMP system. Possible coupling of clearance atrial natriuretic factor receptors to adenylate cyclase/cAMP signal transduction system [J]. J Biol Chem,1990, 265(15): 8566-72.
[148] ANAND-SRIVASTAVA M B, SRIVASTAVA A K, CANTIN M. Pertussis toxin attenuates atrial natriuretic factor-mediated inhibition of adenylate cyclase. Involvement of inhibitory guanine nucleotide regulatory protein [J]. J Biol Chem, 1987, 262(11): 4931-4.
[149] BERL T, MANSOUR J, TEITELBAUM I. ANP stimulates phosphoiipase C in cultured RIMCT cells: roles of protein kinases and G protein [J]. Am J Physiol, 1991, 260(4 Pt 2): F590-5.
[150] RESINK T J, SCOTT-BURDEN T, BAUR U, et al. Atrial natriuretic peptide induces breakdown of phosphatidylinositol phosphates in cultured vascular smooth-muscle cells [J]. Eur J Biochem, 1988, 172(2): 499-505.
[151] MURTHY K S, TENG B Q, ZHOU H, et al. G(i-1)/G(i-2)-dependent signaling by single-transmembrane natriuretic peptide clearance receptor [J]. Am J Physiol Gastrointest Liver Physiol, 2000,278(6): G974-80.
[152] POTTER L R. Phosphorylation-dependent regulation of the guanylyl cyclase-linked natriuretic peptide receptor B: dephosphorylation is a mechanism of desensitization [J].Biochemistry, 1998, 37(8): 2422-9.
[153] POTTER L R, HUNTER T. A constitutively "phosphorylated" guanylyl cyclase-linked atrial natriuretic peptide receptor mutant is resistant to desensitization [J]. Mol Biol Cell, 1999, 10(6): 1811-20.
[154] FOWKES R C, FORREST-OWEN W, MCARDLE C A. C-type natriuretic peptide (CNP) effects in anterior pituitary cell lines: evidence for homologous desensitisation of CNP-stimulated cGMP accumulation in alpha T3-1 gonadotroph-derived cells [J]. J Endocrinol, 2000, 166(1): 195-203.
[155] POTTER L R, GARBERS D L. Protein kinase C-dependent desensitization of the atrial natriuretic peptide receptor is mediated by dephosphorylation [J]. J Biol Chem, 1994, 269(20):14636-42.
[156] HANEDA M, KIKKAWA R, MAEDA S, et al. Dual mechanism of angiotensin II inhibits ANP-induced mesangial cGMP accumulation [J]. Kidney Int, 1991,40(2): 188-94.
[157] ABBEY S E, POTTER L R. Vasopressin-dependent inhibition of the C-type natriuretic peptide receptor, NPR-B/GC-B, requires elevated intracellular calcium concentrations [J]. J Biol Chem, 2002, 277(45): 42423-30.
[158] ABBEY S E, POTTER L R. Lysophosphatidic acid inhibits C-type natriuretic peptide activation of guanylyl cyclase-B [J]. Endocrinology, 2003, 144(1): 240-6.
[159] ABBEY-HOSCH S E, CODY A N, POTTER L R. Sphingosine-1-phosphate inhibits C-type natriuretic peptide activation of guanylyl cyclase B (GC-B/NPR-B) [J]. Hypertension, 2004, 43(5):1103-9.
[160] CHR1SMAN T D, PERKINS D T, GARBERS D L. Identification of a potent serum factor that causes desensitization of the receptor for C-Type natriuretic peptide [J]. Cell Commun Signal,2003, 1(1): 4.
[161] CROOK R B, CHANG A T. Differential regulation of natriuretic peptide receptors on ciliary body epithelial cells [J]. Biochem J, 1997, 324 ( Pt 1)(49-55.
[162] JAISWAL R K. Endothelin inhibits the atrial natriuretic factor stimulated cGMP production by activating the protein kinase C in rat aortic smooth muscle cells [J]. Biochem Biophys Res Commun, 1992, 182(1): 395-402.
[163] POTTER L R, HUNTER T. Activation of protein kinase C stimulates the dephosphorylation of natriuretic peptide receptor-B at a single serine residue: a possible mechanism of heterologous desensitization [J]. J Biol Chem, 2000, 275(40): 31099-106.
[164] POTTHAST R, ABBEY-HOSCH S E, ANTOS L K, et al. Calcium-dependent dephosphorylation mediates the hyperosmotic and lysophosphatidic acid-dependent inhibition of natriuretic peptide receptor-B/guanylyl cyclase-B [J]. J Biol Chem, 2004, 279(47): 48513-9.
[165] ABBEY-HOSCH S E, SMIRNOV D, POTTER L R. Differential regulation of NPR-B/GC-B by protein kinase c and calcium [J]. Biochem Pharmacol, 2005, 70(5): 686-94.
[166] CHARLES C J, ESP1NER E A, NICHOLLS M G, et al. Clearance receptors and endopeptidase 24.11: equal role in natriuretic peptide metabolism in conscious sheep [J]. Am J Physiol, 1996, 271(2 Pt 2): R373-80.
[167] SMITH M W, ESP1NER E A, YANDLE T G, et al. Delayed metabolism of human brain natriuretic peptide reflects resistance to neutral endopeptidase [J]. J Endocrinol, 2000, 167(2): 239-46.
[168] ABASSI Z A, TATE J, HUNSBERGER S, et al. Pharmacokinetics of ANF and urodilatin during cANF receptor blockade and neutral endopeptidase inhibition [J]. Am J Physiol, 1992,263(5 Pt1):E870-6.
[169] FAN D, BRYAN P M, ANTOS L K, et al. Down-regulation does not mediate natriuretic peptide-dependent desensitization of natriuretic peptide receptor (NPR)-A or NPR-B: guanylyl cyclase-linked natriuretic peptide receptors do not internalize [J]. Mol Pharmacol, 2005, 67(1):174-83.
[170] MORISH1TA Y, SANO T, ANDO K, et al. Microbial polysaccharide, HS-142-1,competitively and selectively inhibits ANP binding to its guanylyl cyclase-containing receptor [J].Biochem Biophys Res Commun, 1991, 176(3): 949-57.
[171] SANO T, IMURA R, MOR1SH1TA Y, et al. HS-142-1, a novel polysaccharide of microbial origin, specifically recognizes guanylyl cyclase-linked ANP receptor in rat glomeruli [J]. Life Sci,1992,51(18): 1445-51.
[172] POIRIER H, LABRECQUE J, DESCHENES J, et al. Allotopic antagonism of the non-peptide atrial natriuretic peptide (ANP) antagonist HS-142-1 on natriuretic peptide receptor NPR-A [J]. Biochem J, 2002, 362(Pt 1): 231-7.
[173] DELPORTE C, WINAND J, POLOCZEK P, et al. Discovery of a potent atrial natriuretic peptide antagonist for ANPA receptors in the human neuroblastoma NB-OK-1 cell line [J]. Eur J Pharmacol, 1992,224(2-3): 183-8.
[174] VON GELDERN T W, BUDZIK G P, DILLON T P, et al. Atrial natriuretic peptide antagonists: biological evaluation and structural correlations [J]. Mol Pharmacol, 1990, 38(6):771-8.
[175] PANDEY K N. Biology of natriuretic peptides and their receptors [J]. Peptides, 2005, 26(6): 901-32.
[176] CERMAK R, KLETA R, FORSSMANN W G, et al. Natriuretic peptides increase a K+ conductance in rat mesangial cells [J]. Pflugers Arch, 1996, 431(4): 571-7.
[177] KOURIE J I. Calcium dependence of C-type natriuretic peptide-formed fast K(+) channel [J]. Am J Physiol, 1999, 277(1 Pt 1): C43-50.
[178] SANSOM S C, STOCKAND J D, HALL D, et al. Regulation of large calcium-activated potassium channels by protein phosphatase 2A [J]. J Biol Chem, 1997, 272(15): 9902-6.
[179] GUO H S, CAI Z X, ZHENG H F, et al. Role of calcium-activated potassium currents in CNP-induced relaxation of gastric antral circular smooth muscle in guinea pigs [J]. World J Gastroenterol, 2003, 9(9): 2054-9.
[180] BANKS M, WEI C M, KIM C H, et al. Mechanism of relaxations to C-type natriuretic peptide in veins [J]. Am J Physiol, 1996, 271(5 Pt 2): H1907-11.
[181] HIRSCH J R, MEYER M, MAGERT H J, et al. cGMP-dependent and -independent inhibition of a K+ conductance by natriuretic peptides: molecular and functional studies in human proximal tubule cells [J]. J Am Soc Nephrol, 1999, 10(3): 472-80.
[182] DIXON D B, COPENHAGEN D R. Metabotropic glutamate receptor-mediated suppression of an inward rectifier current is linked via a cGMP cascade [J]. J Neurosci, 1997, 17(23): 8945-54.
[183] KANWAL S, ELMQUIST B J, TRACHTE G J. Atrial natriuretic peptide inhibits evoked catecholamine release by altering sensitivity to calcium [J]. J Pharmacol Exp Ther, 1997, 283(2):426-33.
[184] ISALES C M, LEWICKI J A, NEE J J, et al. ANP-(7-23) stimulates a DHP-sensitive Ca2+ conductance and reduces cellular cAMP via a cGMP-independent mechanism [J]. Am J Physiol,1992, 263(2 Pt 1):C334-42.
[185] SINGER I, EPSTEIN M. Potential of dopamine A-1 agonists in the management of acute renal failure [J]. Am J Kidney Dis, 1998, 31(5): 743-55.
[186] GREEN A K, STRATTON R C, SQUIRES P E, et al. Atrial natriuretic peptide attenuates elevations in Ca2+ and protects hepatocytes by stimulating net plasma membrane Ca2+ efflux [J].J Biol Chem, 2007,282(47): 34542-54.
[187] ROSE R A, ANAND-SRIVASTAVA M B, GILES W R, et al. C-type natriuretic peptide inhibits L-type Ca2+ current in rat magnocellular neurosecretory cells by activating the NPR-C receptor [J]. J Neurophysiol, 2005, 94(1): 612-21.
[188] ROSE R A, LOMAX A E, KONDO C S, et al. Effects of C-type natriuretic peptide on ionic currents in mouse sinoatrial node: a role for the NPR-C receptor [J]. Am J Physiol Heart Circ Physiol, 2004, 286(5): H1970-7.
[189] LEE B, LAYCHOCK S G. Atrial natriuretic peptide and cyclic nucleotides affect glucose-induced Ca2+ responses in single pancreatic islet beta-cells: correlation with (Ca[2+] + Mg2+)-ATPase activity [J]. Diabetes, 1997,46(8): 1312-8.
[190] YOSHIZUMI M, HOUCHI H, TSUCHIYA K, et al. Atrial natriuretic peptide stimulates Na+-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes [J]. FEBS Lett, 1997, 419(2-3): 255-8.
[191] FELDER R A, FELDER C C, EISNER G M, et al. The dopamine receptor in adult and maturing kidney [J]. Am J Physiol, 1989, 257(3 Pt 2): F315-27.
[192] KANTOCI D, WECHTER W J, MURRAY E D, JR., et al. Endogenous natriuretic factors 6: the stereochemistry of a natriuretic gamma-tocopherol metabolite LLU-alpha [J]. J Pharmacol Exp Ther, 1997, 282(2): 648-56.
[193] O'BRODOVICH H, RAFII B, PERLON P. Arginine vasopressin and atrial natriuretic peptide do not alter ion transport by cultured fetal distal lung epithelium [J]. Pediatr Res, 1992,31(4 Pt 1): 318-22.
[194] ROSE R A, HATANO N, OHYA S, et al. C-type natriuretic peptide activates a non-selective cation current in acutely isolated rat cardiac fibroblasts via natriuretic peptide C receptor-mediated signalling [J]. J Physiol, 2007, 580(Pt 1): 255-74.
[195] NOVAIRA H J, ORNELLAS D S, ORTIGA-CARVALHO T M, et al. Atrial natriuretic peptide modulates cystic fibrosis transmembrane conductance regulator chloride channel expression in rat proximal colon and human intestinal epithelial cells [J]. J Endocrinol, 2006, 189(1): 155-65.
[196] PIGGOTT L A, HASSELL K A, BERKOVA Z, et al. Natriuretic peptides and nitric oxide stimulate cGMP synthesis in different cellular compartments [J]. J Gen Physiol, 2006, 128(1):3-14.
[1] Todd PA, Sorkin EM. Diclofenac sodium, a reappraisal of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. Drugs 1988; 35: 244-285.
[2] Dawood MY. Nonsteroidal antiinflammatory drugs and reproduction. Am J Obstet Gynecol 1993; 169: 1255-1265.
[3] Small RE. Diclofenac sodium. Clin Pharmacol 1989; 8: 545-558.
[4] Vane JR. Introduction: mechanism of action of NSAIDs. Br J Rheumatol 1996; 35: 1-3.
[5] Tonussi CR, Ferreira SH. Mechanism of diclofenac analgesia: direct blockade of inflammatory sensitization. Euro J Pharmacol 1994; 251: 173-179.
[6] Asomoza-Espinosa R, Alonso-L(?)pez R, Mixcoatl-Zecuatl T, Aguirre-Bafiuelos P, Torres-Lopez JE, Granados-Soto V. Sildenafil increases diclofenac antinociception in the formalin test.Euro J Pharmacol 2001; 418: 195-200.
[7] Alves D, Duarte I. Involvement of ATP-sensitive K~+ channels in the peripheral antinociceptive effect induced by dipyrone. Euro J Pharmacol 2002; 444: 47-52.
[8] Ortiz MI, Torres-Lopez JE, Casta(?)eda-Hem(?)ndez G, Rosas R, Vidal-Cant(?) GC, Granados-Soto V. Pharmacological evidence for the activation of K~+ channels by diclofenac. Euro J Pharmacol 2002; 438: 85-91.
[9] Voilley N, de Weille J, Mamet J, Lazdunski M. Nonsteroid anti-inflammatory drugs inhibit both the activity and the inflammation-induced expression of acid-sensing ion channels in nociceptors. J Neurosci 2001; 21: 8026-8033.
[10] Lee HM, Kim HI, Shin YK, Lee CS, Park M, Song JH. Diclofenac inhibition of sodium currents in rat dorsal root ganglion neurons. Brain Res 2003; 992: 120-127.
[11] Liu LY, Hu CL, Ma LJ, Zhang ZH, Mei YA. ET-1 inhibits B-16 murine melanoma cell migration by decreasing K~+ currents. Cell Motil Cytoskeleton 2004; 58: 127-136.
[12] Liu LY, Fei XW, Li ZM, Zhang ZH, Mei YA. Diclofenac, a nonsteroidal anti-inflammatory drug, activates the transient outward K~+ current in rat cerebellar granule cells.Neuropharmacology 2005; 48: 918-926.
[13] Occhiodoro T, Bernheim L, Liu JH, Bijlenga P, Sinnreich M, Bader CR, et al. Cloning of a human ether-a-go-go potassium channel expressed in myoblasts at the onset of fusion. FEBS Lett 1998; 434: 177-182.
[14] Bijlenga P, Liu JH, Espinos E, Haenggeli CA, Fischer-Lougheed J, Bader CR, et al. T-type alH Ca~(2+) channels are involved in Ca~(2+) signaling during terminalH Ca~(2+) channels are involved in Ca~(2+) signaling during terminal differentiation (fusion) of human myoblasts. Proc Natl Acad Sci USA 2000; 97: 7627-7632.
[15] Fischer-Lougheed J, Liu JH, Espinos E, Mordasini D, Bader CR, Belin D, et al. Human myoblast fusion requires expression of functional inward rectifier Kir2.1 channels. J Cell Biol 2001; 153: 677-685.
[16] Zhou MO, Liu Z, Hu CL, Zhang ZH, Mei YA. Developmental Regulation of a Na~+-activated Fast Outward K~+ Current in Rat Myoblasts. Cell Physiol Biochem 2004; 14: 225-230.
[17] Lu BX, Liu LY, Liao L, Zhang ZH, Mei YA. Inhibition of Na~+ channel currents in rat myoblasts by 4-aminopyridine. Toxicol Appl Pharm 2005; 207: 275-282.
[18] Kuo CC, Huang RC, Lou BS. Inhibition of Na~+ current by diphenhydramine and other diphenyl compounds: molecular determinants of selective binding to the inactivated channels.Mol Pharmacol 2000; 57: 135-143.
[19] Yang YC, Kuo CC. An Inactivation Stabilizer of the Na~+ Channel Acts as an Opportunistic Pore Blocker Modulated by External Na~+. J Gen Physiol 2005; 125: 465-481.
[20] Fozzard HA, Hanck DA. Structure and function of voltage-dependent sodium channels: comparison of brainⅡ and cardiac isoforms. Physiol Rev 1996; 76: 887-926.
[21] Catterall WA. From ionic current to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron 2000; 26: 13-25.
[22] Nuss HB, Tomaselli GF, Marban E. Cardiac sodium channels (hH1) are intrinsically more sensitive to block by lidocaine than are skeletal muscle (μ1) channels. J Gen Physiol 1995; 106:1193-1209.
[23] Li RA, Ennis IL, Tomaselli GF, Marban E. Structural basis of differences in isoform-specific gating and lidocaine blocking between cardiac and skeletal muscle sodium channels. Mol Pharmacol 2002; 61: 136-141.
[24] Goldin AL. Resurgence of sodium channel research. Annu Rev Physiol 2001; 63: 871-894.
[25] Goldin AL. Diversity of Mammalian Voltage-Gated Sodium Channels. Ann NY Acad Sci 1999; 868:38-50.
[26] Butterworth JF, Strichartz GR. Molecular mechanisms of local anesthesia: a review. Anesthesiology 1990; 72: 711-734.
[27] Laerum E, Ommundsen OE, Gronseth JE, Christiansen A, Fagertun HE. Oral diclofenac in the prophylactic treatment of recurrent renal colic. A double-blind comparison with placebo.Eur Urol 1995; 28: 108-111.
[28] Laerum E, Murtagh J. Renal colic and recurrent urinary calculi. Management and prevention. Aust Fam Physician 2001; 30: 36-41.
[29] Jett MF, Ramesha CS, Brown CD, Chiu S, Emmett C, Voronin T, et al. Characterization of the analgesic and anti-inflammatory activities of ketorolac and its enantiomers in the rat. J Pharmacol Exp Therap 1999; 288: 1288-1297.