Endothelial function and hypertension

Purpose of review Endothelial dysfunction, in particular a reduced vascular availability of endothelium-derived nitric oxide, has been analysed in numerous experimental and clinical studies as a potential mechanism mediating the adverse vascular effects of hypertension. This paper outlines some notable studies in this dynamic field published recently. Recent findings The understanding of mechanisms underlying endothelial dysfunction in hypertension has been substantially advanced recently. Increased oxidant stress is thought to represent a major mechanism leading to reduced vascular availability of endothelium-derived nitric oxide. Vascular nicotinamide adenine dinucleotide phosphate oxidases, uncoupled nitric oxide synthase and xanthine oxidase have been identified as major sources of reactive oxygen species in hypertension. Endothelial dysfunction has been implicated in the macrovascular complications of hypertension, such as stroke or myocardial infarction, coronary microvascular dysfunction and increased arterial stiffness, probably at least partly resulting from loss of the antiatherogenic and vasculoprotective effects of endothelium-derived nitric oxide. Summary Recent research on endothelial dysfunction supports its clinical significance in hypertension, and has led to important insights into the pathophysiology of the disease. These observations suggest that targeting endothelial dysfunction, in particular reduced nitric oxide availability, would exert beneficial effects in hypertensive patients. This concept needs further evaluation in clinical studies.