Abstract
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.
Original language | English |
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Pages (from-to) | 347-360 |
Number of pages | 14 |
Journal | Expert Review of Clinical Pharmacology |
Volume | 3 |
Issue number | 3 |
DOIs | |
Publication status | Published - May 2010 |
All Science Journal Classification (ASJC) codes
- Pharmacology, Toxicology and Pharmaceutics(all)
- Pharmacology (medical)