Endothelial function and oxidant stress

• Type of Material: Article
• Authors: David Harrison, Emory University
• Language: English
• Date: 1997-11-01
• Publisher: WILEY
• Publication Version: Final Published Version
• Copyright Statement: © 1997 The Authors Clinical Cardiology Published by Wiley Periodicals LLC
• License: Creative Commons Attribution-NonCommercial 4.0 International
• Final Published Version (URL): https://doi.org/10.1002%2Fj.1932-8737.1997.tb00007.x
• Title of Journal or Parent Work: CLINICAL CARDIOLOGY
• Volume: 20
• Issue: 11
• Start Page: 11
• End Page: 17
• Keywords: SUPEROXIDE ANION PRODUCTION; BLOOD-FLOW; nitric oxide; atherosclerosis; endothelial function; EXPRESSION; CELLS; ATHEROSCLEROSIS; RELAXING FACTOR; Cardiac & Cardiovascular Systems; NADPH OXIDASE; superoxide dismutase; NITRIC-OXIDE; VASCULAR SMOOTH-MUSCLE; Cardiovascular System & Cardiology; Life Sciences & Biomedicine; hypertension; MYOCARDIAL-INFARCTION; Science & Technology; angiotensin II; superoxide anion
• Research Categories: Health Sciences, Medicine and Surgery; Biology, Cell

Abstract

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.