Endothelial dysfunction in hypertension

Endothelium can deeply influence vascular tone and structure. The main endo thelium derived factor is nitric oxide, which is not only a potent vasodila tor but also inhibits platelet aggregation, smooth muscle cell migration an d proliferation, monocyte adhesion and adhesion molecule expression, thus p rotecting the vessel wall against the development of atherosclerosis and th rombosis. In human hypertension, endothelial dysfunction has been documente d in peripheral and coronary macro and microcirculation and in renal circul ation. Impaired endothelium-dependent vasodilation associated with essentia l hypertension seems to be a primary phenomenon, since it can be detected i n the offspring of essential hypertensive patients, shows no clear correlat ion with blood pressure value, and is not normalized by the mere reduction of blood pressure. The phenomenon responsible for endothelial alteration in essential hypertensive patients seems to be the activation of an alternati ve pathway involving cyclooxygenase which reduces NO availability through p roduction of oxidative stress. This alteration in the NO pathway could be t he main mechanism through which a dysfunctional endothelium could be a prom oter of atherosclerosis and thrombosis in essential hypertension.