Vasomotion of coronary arteries: from nitrates to nitric oxide.

Abstract

The vascular endothelium is a source of substances particularly nitric oxide that act in a paracrine fashion either to contract or relax smooth muscle cells and this function is disturbed in atherosclerotic arteries. The endothelium derived nitric oxide contribute in the basal vasomotor tone of epicardial normal and atheromatous coronary coronary arteries, and of atheromatous coronary stenoses in patients with stable angina. Nitrates, by acting indirectly to increase cGMP in smooth muscle cells, dilate most coronary stenoses and normal coronary segments, decrease left ventricular afterload and diastolic filling pressure and improve the distribution of coronary flow to subendocardial zone. Large and small epicardial coronary vessels responded differently to endothelium-dependent and independent vasodilators.