Acute effects of angiotensin-converting enzyme inhibition on coronary vasomotion in hypertensive patients.

Abstract

Coronary vasodilator responses to pharmacological (acetylcholine) and physiological (cold pressor test and flow dependent dilation) stimuli are impaired in hypertensive patients. The ability of angiotensin-converting enzyme inhibitors to restore normal coronary responses in hypertension and the potential mechanisms involved are examined. In spontaneously hypertensive rats, angiotensin-converting enzyme inhibitors prevent impairment of endothelial-dependent relaxation of arterial rings in response to acetylcholine; in dogs, intracoronary infusion of an angiotensin-converting enzyme inhibitor dilates epicardial arteries and enhances coronary blood flow. In hypertensive patients with normal coronary arteries, intravenous administration of the angiotensin-converting enzyme inhibitor perindoprilat changes constriction of coronary arteries to dilation in response to the cold pressor test, and the absence of flow-dependent dilation becomes a normal response. In addition, maximal coronary blood flow induced by papaverine is enhanced by angiotensin-converting enzyme inhibition and minimal coronary resistance is reduced. It is concluded that both animal and human studies have demonstrated that angiotensin-converting enzyme inhibitors may acutely reverse the abnormalities of coronary vasomotion in arterial hypertension. However, not all the mechanisms responsible are fully understood and further studies are needed, particularly to determine the exact role of nitric oxide, bradykinin and oxygen-derived free radicals.