Hypertension, Vol 6, 92-99, Copyright © 1984 by American Heart Association
T Taylor, TJ Moore, NK Hollenberg and GH Williams
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)
ARTICLES
Converting-enzyme inhibition corrects the altered adrenal response to angiotensin II in essential hypertension
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