Regulation of cardiovascular TRP channel functions along the NO–cGMP–PKG axis
Regulation of cardiovascular TRP channel functions along the NO–cGMP–PKG axis
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DOI：
10.1586/ecp.10.15
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发表时间：
2010-05
影响因子：
4.4
通讯作者：
R. Inoue;Juan Shi;Zhong Jian;Y. Imai
中科院分区：
文献类型：
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作者：
R. Inoue;Juan Shi;Zhong Jian;Y. Imai
越来越多的证据表明，一氧化氮（NO）-cGMP-PKG信号通路通过抑制Ca 2+动力学在心血管（CV）反应及其紊乱的负性调节中发挥核心作用。其他证据也揭示了这种信号传导对某些CV功能的刺激作用。近年来，瞬时受体电位（TRP）通道作为参与CV生理和病理生理的非电压门控Ca 2+通道而受到广泛关注。现有的信息表明，这些通道通过PKG介导的磷酸化和S-亚硝基化，分别进行抑制和激活NO，也作为上游调节剂，以促进内皮NO的生产。本文综述了NO-cGMP-PKG信号通路在TRP通道功能调节中的作用及其相关生理和病理生理机制。
There is growing body of evidence that nitric oxide (NO)–cGMP–PKG signaling plays a central role in negative regulation of cardiovascular (CV) responses and its disorders through suppressed Ca2+ dynamics. Other lines of evidence also reveal the stimulatory effects of this signaling on some CV functions. Recently, transient receptor potential (TRP) channels have received much attention as non-voltage-gated Ca2+ channels involved in CV physiology and pathophysiology. Available information suggests that these channels undergo both inhibition and activation by NO via PKG-mediated phosphorylation and S-nitrosylation, respectively, and also act as upstream regulators to promote endothelial NO production. This review summarizes the roles of NO–cGMP–PKG signaling pathway, particularly in regulating TRP channel functions with their associated physiology and pathophysiology.