AUREA JOSE, M.D.; J. RICHARD CROUT, M.D., F.A.C.P.; NORMAN M. KAPLAN, M.D., F.A.C.P.
Possible mechanisms causing suppressed plasma renin activity (PRA) in about 25% of patients with essential hypertension are examined. Seven patients with normally responsive PRA were compared to five patients with suppressed PRA. Measurements were made during and after manuevers known to affect the renin-angiotensin system, including shrinkage of plasma volume induced by a low-sodium diet plus upright posture and a moderate fall in blood pressure induced by guanethidine. Sympathetic nervous system involvement was examined by catecholamine excretion and responses to norepinephrine infusion. A relative inhibition of the renin-release mechanism that fails to respond normally to various stimuli is indicated. Suppression of PRA was accompanied by subnormal rise in aldosterone excretion and inability to conserve sodium. This inhibition is associated with expanded extracellular fluid volume but does not appear to be caused by an excess of mineralocorticoid or an intrinsic defect in the sympathetic nervous system.
AUREA JOSE, J. RICHARD CROUT, NORMAN M. KAPLAN. Suppressed Plasma Renin Activity in Essential Hypertension: Roles of Plasma Volume, Blood Pressure, and Sympathetic Nervous System. Ann Intern Med. 1970;72:9–16. doi: 10.7326/0003-4819-72-1-9
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Published: Ann Intern Med. 1970;72(1):9-16.
Cardiology, Coronary Risk Factors, Hypertension, Nephrology, Neurology.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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