Abstract
Endothelial cells play numerous physiologic roles including regulation of vascular tone, regulation of hemostasis and fibrinolysis, regulation of inflammatory processes, and maintenance of a permeability barrier to provide for exchange and active transport of substances into the artery wall. Pathophysiologic stimuli can result in localized alterations in endothelial activity. These changes include increased permeability to plasma lipoproteins, imbalances in local thrombogenic substances causing a prothrombotic state, and release of vasoactive compounds resulting in vasoconstriction. Loss of endothelium-dependent vasodilatation is thought to be an early physiologic event in the development of arteriosclerosis, occurring before morphologic changes in the endothelium can be detected. Much of the effects of healthy endothelium appear to be produced by nitric oxide. Decreased bioavailability of nitric oxide results in endothelial dysfunction, which is the first step in the atherosclerotic process. Risk factor modification and pharmacologic interventions that can reverse endothelial dysfunction have the potential to decrease cardiovascular events in patients at risk.
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