RANDOLPH M. MCCLOY, M.D.; WILLIAM P. BALDUS, M.D.; W. H. J. SUMMERSKILL, D.M.; FRANK T. MAHER, M.D., F.A.C.P.
Fluid retention accompanying advanced cirrhosis is characterized by secondary hyperaldosteronism and increased reabsorption of sodium by the kidney; the nature of the stimulus to increased aldosterone production is uncertain. The augmentation of aldosterone secretion in health resulting from infusion of angiotensin suggests that the latter may function as a trophic hormone for aldosterone (1-3). Whereas infusion of angiotensin causes sodium retention in normal man, patients with cirrhosis may exhibit a natriuretic and diuretic response (2). This paradoxical effect of angiotensin on sodium excretion in cirrhosis has not been explained. An opportunity to investigate the effects of angiotensin on renal function
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MCCLOY RM, BALDUS WP, SUMMERSKILL WHJ, MAHER FT. Angiotensin-induced Natriuresis in Cirrhosis in the Absence of Endogenous Aldosterone Secretion. Ann Intern Med. 1966;64:1271–1276. doi: 10.7326/0003-4819-64-6-1271
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Published: Ann Intern Med. 1966;64(6):1271-1276.
Gastroenterology/Hepatology, Liver Disease.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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