Modulatory Role of Nitric Oxide/cGMP System in Endothelin-1-Induced Signaling Responses in Vascular Smooth Muscle Cells

Author(s): Georgia Kapakos, Ali Bouallegue, Grace Bou Daou, Ashok K. Srivastava

Journal Name: Current Cardiology Reviews

Volume 6 , Issue 4 , 2010

Become EABM
Become Reviewer
Call for Editor


Nitric oxide (NO) is an important vasoprotective molecule that serves not only as a vasodilator but also exerts antihypertrophic and antiproliferative effects in vascular smooth muscle cells (VSMC). The precise mechanism by which the antihypertrophic and antiproliferative responses of NO are mediated remains obscure. However, recent studies have suggested that one of the mechanisms by which this may be achieved includes the attenuation of signal transduction pathways responsible for inducing the hypertrophic and proliferative program in VSMC. Endothelin-1 is a powerful vasoconstrictor peptide with mitogenic and growth stimulatory properties and exerts its effects by activating multiple signaling pathways which include ERK 1/2, PKB and Rho-ROCK. Both cGMP-dependent and independent events have been reported to mediate the effect of NO on these pathways leading to its vasoprotective response. This review briefly summarizes some key studies on the modulatory effect of NO on these signaling pathways and discusses the possible role of cGMP system in this process.

Keywords: Endothelin-1, Nitric oxide, ERK1/2, PKB, VSMC, Proliferation, Hypertrophy, Vasculature, Endothelin-1-Induced, non-prostaglandin, vasculo-protective, vasoconstrictor peptide, nucleotide-binding, biphosphate, phosphatidylinositol-3-kinase, guanylate cyclase, phospholamban, vasoconstrictor, non-hydro-lyzable analogue, angiotensin II, RhoA-ROCK, antiproliferative, hypertrophic, cytoplasmic Ca2+, NADPH-oxidase, triggering

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2010
Published on: 01 March, 2012
Page: [247 - 254]
Pages: 8
DOI: 10.2174/157340310793566055
Price: $65

Article Metrics

PDF: 4