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.
Division of Nephrology and Hypertension, Oregon Health Sciences
University, and Veterans Administration Medical Center, Portland,
OR
APStracts 3:0085F, 1996.
The renin-angiotensin system (RAS) has been implicated in the
pathogenesis of diabetic nephropathy. In diabetes, 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 (IV) angiotensin (Ang)
I and Ang II produced similar increases in mean arterial pressure
(MAP). In contrast, glomerular filtration rate (GFR) declined only in
diabetic rats. Renal plasma flow (RPF) fell in both groups, but
decreased more in diabetic rats. Additional groups were given the
same dose of Ang I directly into the left renal artery, and
hemodynamics were studied in the treated and untreated kidneys. In
contrast to the IV studies, intra-arterial Ang I had no effect on MAP
in either group. The renal hemodynamic effects were similar to those
in IV studies. Additionally, diabetic rats exhibited enhanced
hemodynamic sensitivity in the untreated kidney, suggesting that
renal effects could occur at non-pressor concentrations of
circulating Ang II. Thus, renal (but not systemic) responsiveness to
angiotensins is enhanced in diabetic rats.
Received 7 February 1996; accepted in final form 1 May 1996.
APS Manuscript Number F41-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 May 96