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 subject s and in one group of renovascular hypertensive patients. The former s ubjects 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 min utes) and at a pressor dose (13 ng/kg/min for 15 minutes). Furosemide induced a significant reduction in coronary blood flow (CBF), a signif icant increase in coronary vascular resistance (CVR) and also blunted the increase in CBF during handgrip exercise. Captopril restored CBF a nd CVR to pretreatment values. Infusion of the subpressor dose of AngI I decreased myocardial oxygen supply, both at rest and during exercise ; the pressor dose increased myocardial oxygen supply at rest and blun ted 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 i ncreases in CBF for a given increase in myocardial oxygen requirements . These data suggest that there is a negative interference by abnormal ly high plasma levels AngII with myocardial perfusion and that the Ang II-induced effects on coronary hemodynamics are reversed by converting enzyme inhibition.