Nitric oxide modulates angiotensin ii and norepinephrine dependent
vasoconstriction in the rat kidney.
Parekh, Niranjan, Leszek Dobrowolski, Ai-Ping Zou, and Michael
Steinhausen.
Department of Physiology, University of Heidelberg, Heidelberg,
Germany
APStracts 2:0280R, 1995.
This study compared the vasoconstrictor action of angiotensin II (AII)
and norepinephrine (NE) with different levels of nitric oxide in the
kidney of anesthetized rats. In one series of experiments, the drugs
were infused intravenously and systemic NO content was reduced by a
NO synthase inhibitor, nitro-L-arginine methyl ester (L-NAME). L-NAME
significantly enhanced the renal blood flow (RBF) reduction produced
by AII, from 26 to 49%, but it had no significant effect on the
change in RBF induced by NE. Medullary blood flow was not influenced
by either AII or NE given alone or given after L-NAME. In the second
series of experiments all drugs were infused into the renal artery to
avoid their systemic and hence extrarenal effects. In these
experiments, renal content of NO was increased by the NO donor sodium
nitroprusside (SNP), decreased by L-NAME, or restored by replacing
endogenous NO by exogenous NO (L-NAME + SNP). Effects of both AII and
NE on RBF were similarly and significantly attenuated by SNP (60% of
control), enhanced by L-NAME (200% of control), and restored by L
-NAME + SNP (90% of control, NS). Our results indicate that NO
attenuates the renal vasoconstriction due to AII or NE, and that the
antagonism between vasoconstrictors and NO is not due to a
constrictor-induced production of NO because exogenous and endogenous
NO were equally effective.
Received 20 April 1995; accepted in final form 5 October 1995.
APS Manuscript Number R240-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 November 95