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The vascular endothelium is involved in the release of various vasodilators, including nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor, as well as vasoconstrictors. NO plays an important role in the regulation of vascular tone, inhibition of platelet aggregation, and suppression of smooth muscle cell proliferation. Endothelial dysfunction is the initial step in the pathogenesis of atherosclerosis. Cardiovascular diseases are associated with endothelial dysfunction. It is well known that the grade of endothelial function is a predictor of cardiovascular outcomes. Oxidative stress plays an important role in the pathogenesis and development of cardiovascular diseases. Several mechanisms contribute to impairment of endothelial function. An imbalance of reduced production of NO or increased production of reactive oxygen species, mainly superoxide, may promote endothelial dysfunction. One mechanism by which endothelium-dependent vasodilation is impaired is an increase in oxidative stress that inactivates NO. This review focuses on recent findings and interaction between endothelial function and oxidative stress in cardiovascular diseases.
Higashi et al. (2009) studied this question.