Vascular nitric oxide: Beyond eNOS.

By Yingzi Zhao, P. Vanhoutte, Susan Wai Sum Leung. Journal of Pharmacological Sciences, 2015

748 citations recorded by the source corpus.

As the first discovered gaseous signaling molecule, nitric oxide (NO) affects a number of cellular processes, including those involving vascular cells. This brief review summarizes the contribution of NO to the regulation of vascular tone and its sources in the blood vessel wall. NO regulates the degree of contraction of vascular smooth muscle cells mainly by stimulating soluble guanylyl cyclase (sGC) to produce cyclic guanosine monophosphate (cGMP), although cGMP-independent signaling [S-nitrosylation of target proteins, activation of sarco/endoplasmic reticulum calcium ATPase (SERCA) or production of cyclic inosine monophosphate (cIMP)] also can be involved. In the blood vessel wall, NO is produced mainly from l-arginine by the enzyme endothelial nitric oxide synthase (eNOS) but it can also be released non-enzymatically from S-nitrosothiols or from nitrate/nitrite. Dysfunction in the production and/or the bioavailability of NO characterizes endothelial dysfunction, which is associated with cardiovascular diseases such as hypertension and atherosclerosis.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/b6bfc13ebe1b087b844497282ccf205b20797efd

Citations in the corpus

• Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling (2018, neutral): “For example, in the blood vessels of mammals, NO• produced by endothelial cells is a vasodilator of the underlying smooth muscles (Zhao et al., 2015).”