Abstract
In healthy coronary arteries, the endothelium plays an important role in the regulation of vascular smooth muscle growth and contractility. Furthermore, the endothelium inhibits overt platelet aggregation and prevents the adhesion of white blood cells to, and their infiltration into, the vascular wall. Among the mediators of these functions of endothelial cells, nitric oxide (NO) plays a central role. Moreover, the presence of local kinin-generating enzymatic systems associated with endothelial cells, vascular smooth muscle, platelets, neutrophils and monocytes suggests that bradykinin stimulates endothelial cells to release NO locally. The activation of endothelial cells by bradykinin is inhibited by kininase II, best known as angiotensin converting enzyme (ACE). Hence, ACE inhibitors, in addition to reducing the levels of angiotensin II (a potent stimulus to vascular smooth muscle growth and contraction), cause an amplification of the release of NO and other endothelial mediators that is induced by bradykinin. Independent risk factors for coronary artery disease such as hypertension, diabetes and hypercholesterolaemia reduce the NO-dependent regulation of vascular smooth muscle contractility and growth in otherwise normal cor...Continue Reading
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