Converting-enzyme inhibition corrects the altered adrenal response to angiotensin II in essential hypertension.

Of patients with essential hypertension, 30% to 50% do not modulate adrenal and renovascular responsiveness to angiotensin II (AII) with changes in sodium intake. To define the role of AII in mediating these altered responses, the adrenal and renal vascular responses to AII infusion (0.3, 1.0, 3.0 ng/kg/min) were assessed on a sodium-restricted intake in 31 patients with essential hypertension and 13 normotensive controls before and after 72 hours of converting-enzyme inhibition. Forty percent of the hypertensive patients had a subnormal adrenal response to AII. There were no differences between the normal and abnormal responding hypertensive patients in a number of clinical and biochemical factors except that the "abnormal responders" had a significantly (p less than 0.03) greater control AII level (37 +/- 3 vs 29 +/- 3 pg/ml) and lower control plasma aldosterone level (14 +/- 2 vs 22 +/- 3 ng/dl) than the "normal responders." When a converting-enzyme inhibitor was administered, no change in adrenal responsiveness to AII occurred in the normotensive controls or the hypertensive normal responders. In the hypertensive abnormal responders, both the threshold sensitivity and the entire dose response curve was significantly (p less than 0.01) enhanced following short-term converting-enzyme inhibition. This increased sensitivity could not be explained by differences in AII increment with AII infusions, in basal aldosterone levels, or in blood pressure or basal AII response to converting-enzyme inhibition. Since they occurred whether captopril or enalapril (MK 421) were used, this phenomenon is likely to be a specific effect of converting-enzyme inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)