Enhanced renal sensitivity to angiotensin actions in diabetes mellitus in the rat

Enhanced renal sensitivity to angiotensin actions in diabetes mellitus in the rat Kennefick, Thomas M., Terry T. Oyama, Michele M. Thompson, Jiten P. Vora, and Sharon Anderson. Enhanced renal sensitivity to angiotensin actions in mellitus in the rat. Am. J. PhysioZ. 271 (Renal Fhid ElectroZyte Physiol. 40): F595-F602, 1996.-The (RAS) has been implicated in the pathogenesis of diabetic nephropathy. In , renal RAS components are dysregulated, potentially increasing renal RAS effects. To explore the renal RAS, studies were conducted in control and diabetic rats. In both groups, intravenous angiotensin (ANG) I and ANG II produced similar increases in mean arterial pressure (MAP). In contrast, glomerular filtration rate declined only in diabetic rats. Renal plasma flow fell in both groups but decreased more in diabetic rats. Additional groups were given the same dose ofANG I directly into the left renal artery, and hemodynamics were studied in the treated and untreated kidneys. In contrast to the intravenous studies, intra-arterial ANG I had no effect on MAP in either group. The renal hemodynamic effects were similar to those in intravenous studies. Additionally, diabetic rats exhibited enhanced hemodynamic sensitivity in the untreated kidney, suggesting that renal effects could occur at nonpressor concentrations of circulating ANG II. Thus renal (but not ic) responsiveness to angiotensins http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Renal Physiology The American Physiological Society

Enhanced renal sensitivity to angiotensin actions in diabetes mellitus in the rat

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Publisher
The American Physiological Society
Copyright
Copyright © 1996 the American Physiological Society
ISSN
0363-6127
eISSN
1522-1466
Publisher site
See Article on Publisher Site

Abstract

Kennefick, Thomas M., Terry T. Oyama, Michele M. Thompson, Jiten P. Vora, and Sharon Anderson. Enhanced renal sensitivity to angiotensin actions in mellitus in the rat. Am. J. PhysioZ. 271 (Renal Fhid ElectroZyte Physiol. 40): F595-F602, 1996.-The (RAS) has been implicated in the pathogenesis of diabetic nephropathy. In , renal RAS components are dysregulated, potentially increasing renal RAS effects. To explore the renal RAS, studies were conducted in control and diabetic rats. In both groups, intravenous angiotensin (ANG) I and ANG II produced similar increases in mean arterial pressure (MAP). In contrast, glomerular filtration rate declined only in diabetic rats. Renal plasma flow fell in both groups but decreased more in diabetic rats. Additional groups were given the same dose ofANG I directly into the left renal artery, and hemodynamics were studied in the treated and untreated kidneys. In contrast to the intravenous studies, intra-arterial ANG I had no effect on MAP in either group. The renal hemodynamic effects were similar to those in intravenous studies. Additionally, diabetic rats exhibited enhanced hemodynamic sensitivity in the untreated kidney, suggesting that renal effects could occur at nonpressor concentrations of circulating ANG II. Thus renal (but not ic) responsiveness to angiotensins

Journal

AJP - Renal PhysiologyThe American Physiological Society

Published: Sep 1, 1996

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