Nitric oxide and hypertension

Abstract

Nitric oxide (NO) is a ubiquitous, naturally occurring molecule found in a variety of cell types and organ systems. In the cardiovascular system, NO is important for both normal physiological function and in the pathogenesis of cardiovascular disorders such as essential hypertension and atherosclerosis. Impaired relaxation by acetylcholine was demonstrated in spontaneously hypertensive rats and hypertensive patients, suggesting that endothelium dysfunction caused an abnormal relaxation. Decreased bioavailability of NO has been identified as a major cause of impaired endothelial function. Alterations of NOS expression as well as enhanced NO breakdown by superoxide anion observed in hypertensive condition may principally contribute to the decreased bioavailability of NO. The fact that antihypertensive treatment with calcium channel blocker or angiotensin converting enzyme inhibitors improves NO bioavailability and subsequent endothelium-dependent relaxation in hypertension patients, may be related to an antioxidant activity of these drugs. Thus, further identifying the mechanisms responsible for endothelial dysfunction and designing some drags which restore NO bioavailability may provide more insights into the mechanisms of pathogenesis of hypertension and also be a potential therapeutic strategy for this disease.