Open AccessEndothelial Function and Oxidant Stress
Author(s) -
Harrison David G.
Publication year - 1997
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/j.1932-8737.1997.tb00007.x
Subject(s) - superoxide , superoxide dismutase , nadph oxidase , reactive oxygen species , nitric oxide , medicine , angiotensin ii , oxidative stress , biochemistry , oxidase test , nicotinamide adenine dinucleotide phosphate , hydrogen peroxide , endothelium , endocrinology , enzyme , chemistry , blood pressure
Both endothelial cells and vascular smooth muscle cells are capable of producing reactive oxygen species from a variety of enzymatic sources. In disease states such as atherosclerosis and hypertension, vascular production of these reactive oxygen metabolites can increase substantially. Increases in the production of superoxide anion can lead to decreases in ambient levels of nitric oxide via a facile radical/radical reaction that occurs more rapidly than the reaction of superoxide anion with superoxide dismutase. This phenomenon alters endothelial regulation of vasomotion in a variety of disease conditions. Recent evidence suggests that the major source of vascular superoxide ion and hydrogen peroxide is a membrane‐bound, reduced nicotinamide‐adenine dinucleotide (NADH)‐dependent oxidase. The activity of this enzyme system is regulated by angiotensin II and is elevated following prolonged exposure to nitroglycerin. Alterations of vascular oxidant state caused by angiotensin II may contribute substantially to vascular pathology and may also provide a link between hypertension and atherosclerosis.