AI Article Synopsis
- Nitric oxide (NO) is a key gaseous signaling molecule that regulates various cellular processes, especially in the vascular system.
- NO primarily affects vascular smooth muscle cells by activating soluble guanylyl cyclase (sGC) to produce cGMP, but it can also utilize cGMP-independent pathways.
- Endothelial nitric oxide synthase (eNOS) produces NO from l-arginine in blood vessels, and disruptions in NO production are linked to cardiovascular issues like hypertension and atherosclerosis.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.jphs.2015.09.002 | DOI Listing |
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