Endothelium-derived nitric oxide in the control of tissue perfusion and oxygen supply: physiological and pathophysiological implications.

Since the development of specific NO-synthase inhibitors it has become possible to study the role of NO in the control of local blood flow and tissue oxygenation. Inhibition of NO-synthase induces hypertension and abnormal vasoconstriction, as well as tissue hypoxia and impaired adaptation of blood flow to increased tissue oxygen demands. These functional alterations are similar to those observed in a number of cardiovascular diseases. The present evidence that impaired endothelial function is a pathogenetic factor in the development of cardiovascular diseases is briefly reviewed.