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Effect of Saralasin in Hypertensive Patients on Chronic Hemodialysis

MEYER D. LIFSCHITZ, M.D.; MICHAEL A. KIRSCHENBAUM, M.D.; STEVEN G. ROSENBLATT, M.D.; and RICHARD GIBNEY, M.D.
[+] Article and Author Information

Grant support: in part by Program Project Grant AM-17387, Training Grant AM-07103, and by a grant from Eaton Laboratories.

This paper was presented in part at the Southern Section Meeting of the American Federation for Clinical Research, New Orleans, Louisiana, 27 January 1977.

▸Requests for reprints should be addressed to Meyer D. Lifschitz, M.D.; Department of Medicine, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive; San Antonio, TX 78284.


©1978 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1978;88(1):23-27. doi:10.7326/0003-4819-88-1-23
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Hypertension in patients on chronic hemodialysis is thought to be largely of two types—volume dependent or renin dependent. If renin-dependent hypertension is mediated by angiotensin II, then angiotensin II antagonism should lower blood pressure. To test this hypothesis, the angiotensin II antagonist saralasin was given to 15 hypertensive patients on chronic hemodialysis. Patients were separated into two groups by their blood pressure response. In responders blood pressure was 191/112 mm Hg and fell to 147/85 during saralasin administration (P < 0.01). In contrast, nonresponders had blood pressures of 190/111 mm Hg before and 188/110 during saralasin administration. Five responders subsequently had nephrectomies with normalization of their blood pressures. Plasma renin activity averaged 70 ng/ml · 3 h of angiotensin I in responders and increased to 110 after saralasin (P < 0.05), while nonresponders had values of 21 before and after saralasin. These results offer strong support for the hypothesis that renin-dependent hypertension is an important mechanism in certain patients on chronic hemodialysis and that such patients will respond to angiotensin II antagonism.

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