Skip Navigation LinksHome > May 2003 - Volume 35 - Issue 5 > ENDOTHELIAL DYSFUNCTION IN AGING ‐ ROLE OF NITRIC OXIDE
Medicine & Science in Sports & Exercise:
Nitric Oxide: Role in Combating Disease

ENDOTHELIAL DYSFUNCTION IN AGING ‐ ROLE OF NITRIC OXIDE

Woodman, C R.1

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1University of Missouri, Columbia, MO

Results from several studies indicate that aging impairs endothelial function. The vascular dysfunction induced by aging is associated with blunted vasodilator responses in coronary and peripheral arteries. Vascular endothelium plays an important role in regulating vasodilator responses by synthesizing and releasing a number of vasoactive molecules that diffuse to surrounding vascular smooth muscle causing relaxation. While the mechanism(s) for the detrimental effects of age on endothelium-dependent dilation are not fully understood, it has been hypothesized that aging is associated with a reduction in the production and/or release of nitric oxide (NO). This hypothesis is supported by experimental evidence indicating that vasodilator responses to agonists that stimulate endothelial cell derived NO production (flow, acetylcholine) are impaired in senescent arteries, whereas dilation to an exogenous source of NO (sodium nitroprusside) is not compromised. This hypothesis is also supported by experimental evidence indicating that endothelial nitric oxide synthase (eNOS) protein expression decreases with age in coronary and peripheral arteries. Alternatively, age-associated decrements in NO-mediated vasodilation may be due to enhanced free radical inactivation of NO by superoxide anion. This speculation is supported by experimental evidence that superoxide production is enhanced in senescent coronary arteries. In addition, expression of superoxide dismutase (SOD-1), the primary scavenger of superoxide, is reduced in peripheral arteries from senescent rats. The goal of this presentation is to review these and other studies designed to test the hypothesis that age-induced endothelial dysfunction is due in part to impaired NO-mediated dilation in coronary and peripheral arteries. (Supported by NIH AG-00988)

©2003The American College of Sports Medicine

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