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European Heart Journal 1992 13(Supplement D):50-55; doi:10.1093/eurheartj/13.suppl_D.50
Copyright © 1992 by the European Society of Cardiology.
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© 1992 The European Society of Cardiology

Heterogeneity of endothelial dysfunction in hypertension

T. F. Lüscher

Department of Medicine, Divisions of Clinical Pharmacology and Cardiology and Department of Research, Laboratory of Vascular Research University Hospital Basel, Switzerland

Address for correspondence: Thomas F. Lüscher, MD, Department of Medicine University Hospital, 4031 Basel/Switzerland

The endothelium may play a role as a target and mediator of hypertension. Due to its anatomical position, it is very exposed to mechanical forces; as a source of vasoactive material it may participate in increasing peripheral vascular resistance and in promoting local ischaemia in the heart and brain. Morphological and functional changes in the endothelium occur in experimental and human hypertension. However, the severity of the defect and the mechanisms involved among vascular beds and models of hypertension are heterogeneous. Endothelium-dependent relaxations are impaired in the aorta, carotid artery and in cerebral and mesenteric arterioles in hypertension. In the coronary circulation the defect is less pronounced. The mechanisms involve a reduced formation of nitric oxide, an enhanced production of prostaglandin H2 and an impaired responsiveness of vascular smooth muscle to nitric oxide. The role of endothelin in hypertension is controversial; circulating levels appear unaltered except in the presence of renal failure or atherosclerosis. The local vascular production of endothelin, however, may still be increased. The potentiating effects of threshold concentrations of endothelin on the vasoconstrictor response to noradrenalin are enhanced in hypertension.

Thus, subtle and distinct endothelial function defects occur in hypertension, but not all vascular beds are similarly affected and different mechanisms contribute. Endothelial dysfunction may contribute to increased peripheral resistance, tissue ischaemia and cardiovascular complications.

Key Words: Antihypertensive therapy • endothelin-1 • mechanisms • heterogeneity • nitric oxide


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