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Control of Renal Function by Intrarenal Angiotensin II^*

NIGEL R. LEVENS, ARTHUR E. FREEDLENDER, MICHAEL J. PEACH and ROBERT M. CAREY

Division of Endocrinology and Metabolism, Department of Internal Medicine, and the Department of Pharmacology, University of Virginia School of Medicine Charlottesville, Virginia 22908

Address requests for reprints to: Dr. Robert M. Carey, Box 482, University of Virginia Medical Center, Charlottesville, Virginia 22908.

Abstract

The purpose of this study was to determine if endogenous angiotensin II affects renal function in conscious dogs after sodium restriction. Intrarenal infusion of the angiotensin receptor antagonist saralasin at doses between 0.13 and 2.5 µg/kg·min rapidly attenuated pressor responses produced by systemic injections of angiotensin I over a 90-min period. In contrast, intrarenal infusion of the peptide antagonist at 0.07 µg/ kg·min did not alter the pressor response to injected angiotensin I. Infusion of angiotensin II into the kidney at 0.1 µg/min reduced urine output by 50% and was totally inhibited by simultaneous infusion of 0.07 µg/kg·min saralasin. Intrarenal infusion of saralasin at 0.07 µg/kg·min into sodium-restricted conscious dogs increased effective renal plasma flow, glomerular filtration rate, and sodium, potassium and water excretion, whereas urine osmolarity and free water formation were unchanged. These data demonstrate that saralasin can be effectively confined to the renal mass after intrarenal infusion at a dose capable of inhibiting angiotensin action and that endogenous angiotensin plays an important role in maintaining renal function after sodium restriction.

Footnotes

^* This work was supported by NIH Grants HL-19242 and HL-22306.

Present address: Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26506.

Received June 7, 1982.

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