[Endothelial functions in cardiovascular diseases]

In recent years it has become apparent that endothelial cells have important implications in the regulation of vascular smooth muscle tone, vascular permeability and platelet reactivity. One important physiological feature of these cells is the formation of the endothelium-derived relaxing factor (EDRF). This short-lived compound is a potent vascular smooth muscle relaxant and it also inhibits platelet aggregation and adhesion to the vessel wall. Its active principle seems to be nitric oxide (NO), and consequently it can be regarded as the "endogenous nitrovasodilator". In addition to EDRF, endothelial cells synthesize prostacyclin which also has platelet antiaggregatory and vasodilator properties. A reduced effectiveness of the EDRF mechanism is implicated, especially in those events of the vascular pathophysiology associated with an increased vascular tone or vasospasm. For example, a reduced production and/or action of EDRF has been found in animal models of atherosclerosis as well as in atherosclerotic human coronary arteries. In addition, prostacyclin production is reduced under these conditions. In different animal models of hypertension and diabetes mellitus, endothelium-mediated relaxation is also found to be reduced. In addition, under certain pathophysiological conditions, the endothelium seems to produce vasoconstrictor material.