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Impaired Endothelial Nitric Oxide Bioavailability: A Common Link Between Aging, Hypertension, and Atherogenesis?
Author(s) -
Walsh Thomas,
Donnelly Teresa,
Lyons Declan
Publication year - 2009
Publication title -
journal of the american geriatrics society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.992
H-Index - 232
eISSN - 1532-5415
pISSN - 0002-8614
DOI - 10.1111/j.1532-5415.2008.02051.x
Subject(s) - medicine , nitric oxide , endothelial dysfunction , vasodilation , blood pressure , bioavailability , vascular disease , pathophysiology of hypertension , vasomotor , endothelium , vascular smooth muscle , endocrinology , pharmacology , cardiology , smooth muscle
Endothelial‐derived nitric oxide (NO) is responsible for maintaining continuous vasodilator tone and for regulating local perfusion and systemic blood pressure. It also has significant antiproliferative effects on vascular smooth muscle and platelet anti‐aggregatory effects. Impaired endothelial‐dependent (NO mediated) vasorelaxation is observed in most animal and human models of healthy aging. It also occurs in age‐associated conditions such as atherosclerosis and hypertension. Such “endotheliopathy” increases vascular risk in older adults. Studies have indicated that pharmacotherapeutic intervention with angiotensin‐converting enzyme inhibitors and 3‐hydroxy‐3‐methyl‐glutaryl coenzyme‐A reductase inhibitors may improve NO‐mediated vasomotor function. This review, evaluates the association between impaired endothelial NO bioavailability, accelerated vascular aging, and the age‐associated conditions hypertension and atherogenesis. This is important, because pharmacotherapy aimed at improving endothelial NO bioavailability could modify age‐related vascular disease and transform age into a potentially modifiable vascular risk factor, at least in a subpopulation of older adults.