ARTERIAL HEMODYNAMICS IN HUMAN HYPERTENSION - EFFECTS OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION

Previous studies have shown some distinct hemodynamic alterations in e ssential hypertension, including increased resistance, wave reflection s, and pulse wave velocity and decreased systemic compliance. These ab normalities are completely normalized by nonspecific smooth muscle dil ation with nitroprusside but not by combined alpha- and beta-adrenergi c blockade. The renin-angiotensin system, acting possibly via both cir culating and local tissue effects, is thought to play an important rol e in essential hypertension, so its role in the altered hemodynamics d eserves careful investigation. A hypertensive patient group was compar ed with a normotensive group similar in age, body size, and proportion of men and women. During diagnostic cardiac catheterization, ascendin g aortic micromanometer pressures and electromagnetic flows were measu red in the baseline state. Intravenous captopril of a sufficient dosag e (11 mg) to normalize blood pressure then was given to the hypertensi ve patients while measurements were repeated. From the pressures and f lows, aortic input impedance, wave reflection magnitude, and complianc e were computed. In the hypertensive group, the important hemodynamic alterations consisted of increased peripheral resistance, first zero c rossing of aortic impedance phase angle, and wave reflections and decr eased systemic compliance. Captopril had a pronounced hemodynamic effe ct. It normalized blood pressure, resistance, and impedance phase angl e zero crossing. Compliance, although increased substantially by capto pril, was still slightly lower than normotensive levels. The magnitude of wave reflections, although substantially lowered by angiotensin co nverting enzyme inhibition, was still persistently greater than normal . The present results, together with those previously reported, demons trate that a complex interplay of factors underlies the increased smoo th muscle tone in essential hypertension. Whereas nonspecific smooth m uscle relaxation with nitroprusside is able to completely restore hemo dynamics to a normal state, angiotensin converting enzyme inhibition a lone, beta-adrenergic blockade alone, or combined beta- and alpha-bloc kade cannot do so. Therefore, if one wishes to completely normalize th e hemodynamic alterations produced by hypertension in addition to trea ting the elevated blood pressure, one needs to appreciate the actions of these and other antihypertensive agents and select the appropriate combinations that will yield the desired results.