Circ J 2009; 73: 411 -418 arious vasodilators, including nitric oxide (NO), prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF), as well as vasoconstrictors, are released from the endothelium. 1,2 NO plays an important role in the regulation of vascular tone, inhibition of platelet aggregation, and suppression of vascular smooth muscle cell proliferation. 3,4 Impaired endothelium-dependent vasodilation has been found in the forearm, coronary, and renal vasculature of patients

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... h hypertension, 5-11 dyslipidemia, 12,13 diabetes mellitus, 14-16 and coronary artery diseases. 17-21 Endothelial dysfunction is an early feature of both atherosclerosis and vascular diseases in humans. 22 Improvement or augmentation of endothelial function will prevent the development of atherosclerosis, resulting in a reduction in cardiac events. There are several possible mechanisms for impaired endothelial function in patients with cardiovascular diseases. Decreased NO bioavailability (decreased NO production and/or increased NO inactivation) induces endothelial dysfunction. A balance of endothelium-derived vasodilators, especially NO, and reactive oxygen species (ROS) modulates endothelial function. Therefore, an imbalance of NO and ROS, so-called oxidative stress, is involved in endothelial dysfunction through the inactivation of NO. 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. (Circ J 2009; 73: 411 -418) V REVIEW 412 HIGASHI Y et al.