Coronary hemodynamics and the renin angiotensin system

Coronary hemodynamics were investigated invasively at rest and during handgrip exercise in two groups of mild essential hypertensive subjects and in one group of renovascular hypertensive patients. The former subjects received either furosemide (50 mg/day for one week) to ensure activation of the renin-angiotensin system or an intravenous infusion of angiotensin II (AngII) at a subpressor dose (3 ng/kg/min for 15 minutes) and at a pressor dose (13 ng/kg/min for 15 minutes). Furosemide induced a significant reduction in coronary blood flow (CBF), a significant increase in coronary vascular resistance (CVR) and also blunted the increase in CBF during handgrip exercise. Captopril restored CBF and CVR to pretreatment values. Infusion of the subpressor dose of AngII decreased myocardial oxygen supply, both at rest and during exercise; the pressor dose increased myocardial oxygen supply at rest and blunted the expected increase in myocardial oxygen supply during exercise. Converting-enzyme inhibition in renovascular hypertension caused mean arterial pressure to decrease and CBF to increase significantly. The performance of handgrip exercise after cilazapril resulted in higher increases in CBF for a given increase in myocardial oxygen requirements. These data suggest that there is a negative interference by abnormally high plasma levels AngII with myocardial perfusion and that the AngII-induced effects on coronary hemodynamics are reversed by converting enzyme inhibition.