Endothelial dysfunction: its pathogenic role in atherosclerosis and its reversal by ACE inhibition.

Not so long ago the structure and function of the endothelium were of no concern to physicians intent on preventing atherosclerosis and its life-threatening sequelae in their patients. Unexpectedly, researchers have found that this supposedly inert cell line controls many important processes, including maintenance of blood vessel compliance. During the early stages of atherosclerosis and even before the onset of borderline hypertension, its vasodilative function is impaired because of an increase in its permeability to lipoproteins and other plasma constituents. Oxidized lipoproteins inhibit the release of the vasodilative substance nitric oxide, and angiotensin II degrades bradykinin, a potent stimulator of nitric oxide production in endothelial cells that is known to protect against atherosclerosis. Fortunately, preclinical and clinical study data strongly suggest that therapy with angiotensin-converting enzyme inhibitors can reverse endothelial dysfunction by decreasing angiotensin II levels and increasing bradykinin and, in turn, nitric oxide levels.