HUGH M. WILSON, M.D.; JAMES P. WILSON, M.D.; PAUL E. SLATON, M.D., F.A.C.P.; JOHN H. FOSTER, M.D.; GRANT W. LIDDLE, M.D., F.A.C.P.; JOHN W. HOLLIFIELD, M.D.
This paper was presented in part to The American Federation for Clinical Research, May 1976, Atlantic City, New Jersey.
Grant support: by U.S. Public Health Service Grants: 2 P5O HL14192 and 2 MO1-RR-95 and Veterans Administration Training Grant in Endocrinology and Metabolism TR-72.
▸Requests for reprints should be addressed to John W. Hollifield, M.D.; Department of Endocrinology, Vanderbilt University Hospital; Nashville, TN 37232.
WILSON HM, WILSON JP, SLATON PE, FOSTER JH, LIDDLE GW, HOLLIFIELD JW. Saralasin Infusion in the Recognition of Renovascular Hypertension. Ann Intern Med. 1977;87:36-42. doi: 10.7326/0003-4819-87-1-36
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Published: Ann Intern Med. 1977;87(1):36-42.
Saralasin, an angiotensin II antagonist, was infused into 49 patients with renal artery stenosis, 10 patients with essential hypertension and normal renal arteriograms, and five patients with "low-renin essential hypertension." Renal venous renin and differential renal function studies were used to assess the functional significance of arterial stenoses. "Response" to saralasin, evidenced by a fall in blood pressure during infusion, occurred in no patients with "low renin" hypertension and in only 20% of patients with normal renal arteriograms. In contrast, saralasin "response" occurred in more than 80% of patients with renal artery stenosis and lateralizing functional studies and in 100% of cases of "proven" renovascular hypertension (cure or improvement of hypertension after operative treatment). We suggest that saralasin infusion might be a valuable screening test for the recognition of renovascular hypertension.
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Cardiology, Nephrology, Hypertension, Coronary Risk Factors, Prevention/Screening.
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