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Research Article Free access | 10.1172/JCI115899

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

S C Thomson, F B Gabbai, B J Tucker, and R C Blantz

Department of Medicine, University of California, San Diego 92161.

Find articles by Thomson, S. in: PubMed | Google Scholar

Department of Medicine, University of California, San Diego 92161.

Find articles by Gabbai, F. in: PubMed | Google Scholar

Department of Medicine, University of California, San Diego 92161.

Find articles by Tucker, B. in: PubMed | Google Scholar

Department of Medicine, University of California, San Diego 92161.

Find articles by Blantz, R. in: PubMed | Google Scholar

Published August 1, 1992 - More info

Published in Volume 90, Issue 2 on August 1, 1992
J Clin Invest. 1992;90(2):604–611. https://doi.org/10.1172/JCI115899.
© 1992 The American Society for Clinical Investigation
Published August 1, 1992 - Version history
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Abstract

The hypothesis that renal alpha 2 adrenoceptors influence nephron filtration rate (SNGFR) via interaction with angiotensin II (AII) was tested by renal micropuncture. The physical determinants of SNGFR were assessed in adult male Munich Wistar rats 5-7 d after ipsilateral surgical renal denervation (DNX). DNX was performed to isolate inhibitory central and presynaptic alpha 2 adrenoceptors from end-organ receptors within the kidney. Two experimental protocols were employed: one to test whether prior AII receptor blockade with saralasin would alter the glomerular hemodynamic response to alpha 2 adrenoceptor stimulation with the selective agonist B-HT 933 under euvolemic conditions, and the other to test whether B-HT 933 would alter the response to exogenous AII under conditions of plasma volume expansion. In euvolemic rats, B-HT 933 caused SNGFR to decline as the result of a decrease in glomerular ultrafiltration coefficient (LpA), an effect that was blocked by saralasin. After plasma volume expansion, B-HT 933 showed no primary effect on LpA but heightened the response of arterial blood pressure, glomerular transcapillary pressure gradient, and LpA to AII. The parallel results of these converse experiments suggest a complementary interaction between renal alpha 2-adrenergic and AII systems in the control of LpA.

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