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Abnormal Adrenal Responsiveness and Angiotensin II Dependency in High Renin Essential Hypertension
Robert G. Dluhy, … , Norman K. Hollenberg, Gordon H. Williams
Robert G. Dluhy, … , Norman K. Hollenberg, Gordon H. Williams
Published November 1, 1979
Citation Information: J Clin Invest. 1979;64(5):1270-1276. https://doi.org/10.1172/JCI109582.
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Research Article

Abnormal Adrenal Responsiveness and Angiotensin II Dependency in High Renin Essential Hypertension

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Abstract

Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na+/100 meq K+ diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24±6 ng/ml per h) and significantly smaller plasma aldosterone increments 47 ± 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 ± 1 ng/ml per h; plasma aldosterone = 87 ± 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 μg/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (−15 ± 3 mm Hg) was significantly greater than in the normal adrenal responsive group (−3 ± 2 mm Hg) (P < 0.02).

Authors

Robert G. Dluhy, Sam Z. Bavli, Frank K. Leung, Harold S. Solomon, Thomas J. Moore, Norman K. Hollenberg, Gordon H. Williams

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