Reactive Oxygen Species, Nitric Oxide and Hypertensive Endothelial Dysfunction

Endothelial dysfunction, a hallmark of many vascular diseases such as diabetes mellitus, atherosclerosis and essential hypertension, refers to significant impairment of a majority of endothelial activities e.g. modulation of vasomotor tone and inhibition of smooth muscle cell proliferation and/or migration. Several factors including increased synthesis of vasoconstrictor agents through the cyclooxygenase pathway and dysregulation of the gene encoding endothelial type of nitric oxide synthase in endothelium have been proposed to account for this defect in hypertensive subjects. However, a growing body of evidence has recently implicated diminished bio-availability of nitric oxide (NO), the most important endogenous vasodilator agent, due to excessive synthesis or reduced destruction of reactive oxygen species (ROS) in the pathogenesis of hypertensive endothelial dysfunction. Hence, this review aims to summarize the mechanisms by which vascular cells produce NO and ROS, to highlight the molecular mechanisms underlying the pathogenesis of hypertensive endothelial dysfunction with particular reference to interactions between ROS and NO, and finally to discuss the reversal of hypertensive endothelial dysfunction.