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Abstract
As the major regulator of vascular homeostasis, the endothelium exerts a number of
vasoprotective effects, such as vasodilation, suppression of smooth muscle cell growth,
and inhibition of inflammatory responses. Many of these effects are largely mediated
by nitric oxide, the most potent endogenous vasodilator. Nitric oxide opposes the
effects of endothelium-derived vasoconstrictors and inhibits oxidation of low-density
lipoprotein. A defect in the production or activity of nitric oxide leads to endothelial
dysfunction, signaled by impaired endothelium-dependent vasodilation. Accumulating
evidence suggests that endothelial dysfunction is an early marker for atherosclerosis
and can be detected before structural changes to the vessel wall are apparent on angiography
or ultrasound. Many of the risk factors that predispose to atherosclerosis can also
cause endothelial dysfunction, and the presence of multiple risk factors has been
found to predict endothelial dysfunction. A number of clinical trials have shown that
3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) improve
endothelial dysfunction in patients with coronary risk factors beyond what could be
attributed to their impact on plasma lipids. Studies have elucidated several possible
mechanisms by which statin therapy may improve endothelial dysfunction, including
upregulation of nitric oxide production or activity and reduction of oxidative stress.