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Nitric oxide is mediated in mammals by the calcium-calmodulin controlled isoenzymes eNOS (endothelial NOS) and nNOS (neuronal NOS). [2] The inducible isoform, iNOS, involved in immune response, binds calmodulin at physiologically relevant concentrations, and produces NO as an immune defense mechanism, as NO is a free radical with an unpaired ...
7-Nitroindazole, or 7-NI, is a heterocyclic small molecule containing an indazole ring that has been nitrated at the 7 position. Nitroindazole acts as a selective inhibitor for neuronal nitric oxide synthase, a hemoprotein enzyme that, in neuronal tissue, converts arginine to citrulline and nitric oxide (NO). [1]
Endothelial NOS (eNOS), also known as nitric oxide synthase 3 (NOS3) or constitutive NOS (cNOS), is an enzyme that in humans is encoded by the NOS3 gene located in the 7q35-7q36 region of chromosome 7. [5]
Biological functions of nitric oxide are roles that nitric oxide plays within biology. Nitric oxide (nitrogen monoxide) is a molecule and chemical compound with chemical formula of N O. In mammals including humans, nitric oxide is a signaling molecule involved in several physiological and pathological processes. [1]
A nitrovasodilator is a pharmaceutical agent that causes vasodilation (widening of blood vessels) by donation of nitric oxide (NO), [1] and is mostly used for the treatment and prevention of angina pectoris. This group of drugs includes nitrates (esters of nitric acid), which are reduced to NO in the body, as well as some other substances.
The main cause of endothelial dysfunction is impaired bioavailability of nitric oxide. [ 1 ] In addition to acting as a semipermeable membrane , the endothelium is responsible for maintaining vascular tone and regulating oxidative stress by releasing mediators, such as nitric oxide, prostacyclin and endothelin , and by controlling local ...
Inhibition of DDAH activity causes methylarginines to accumulate, blocking nitric oxide(NO) synthesis and causing vasoconstriction. [4] An impairment of DDAH activity appears to be involved in the elevation of plasma ADMA, and impairment of vascular relaxation observed in humans with cardiovascular disease or risk factors (such as hypercholesterolemia, diabetes mellitus, and insulin resistance).
Rho-kinase also decreases nitric oxide synthase activity, which reduces nitric oxide concentrations. [3] Lower levels of nitric oxide are present in spastic coronary arteries. [ 4 ] L-type calcium channel expression increases in spastic vascular smooth muscle cells, which could result in excessive calcium influx, and hypercontraction.