Verapamil abolishes the preglomerular response to angiotensin ii
during intrarenal nitric oxide synthesis inhibition.
Schnackenberg, Christine G., and Joey P. Granger.
Department of Physiology and Biophysics, University of Mississippi
Medical Center
APStracts 3:0409R, 1996.
We have recently reported that intrarenal nitric oxide (NO) synthesis
inhibition exaggerates the preglomerular vasoconstrictor response
more than the postglomerular response to angiotensin II (ANG II) in
dogs. Previous studies have suggested that preglomerular
vasoconstriction may be more dependent upon extracellular calcium
than postglomerular vasoconstriction. The purpose of this study is to
determine whether the enhanced preglomerular response to ANG II
during intrarenal NO synthesis inhibition occurs through voltage
-gated calcium channels. In three groups of anesthetized dogs with
stop-flow kidneys, the renal hemodynamic response to intrarenal ANG
II infusion (2.0 ng/kg/min) was determined. Renal artery pressure was
servo-controlled at 80 +/- 1 mmHg and glomerular filtration rate was
zero. In vehicle-treated dogs, ANG II decreased renal blood flow
(RBF) by 29 % and increased glomerular hydrostatic pressure (Pg) by
2.7 +/- 1.9 mmHg. Postglomerular vascular resistance increased by
51%, while preglomerular resistance was unchanged in response to ANG
II. In dogs pretreated with an intrarenal infusion of L-NAME (5
[mu]g/kg/min) for 60 minutes, ANG II decreased RBF by 36 % and
decreased Pg 4.4 +/- 2.9 mmHg. In contrast to the vehicle treated
group, preglomerular resistance increased by 261 % and postglomerular
resistance increased by 48 % after ANG II infusion in the L-NAME
treated group. In dogs pretreated with an intrarenal infusion of L
-NAME and verapamil (50 [mu]g/min) for 60 minutes, the renal
hemodynamic response to ANG II was similar to the response in the
vehicle-treated dogs. ANG II decreased RBF by 25 % and decreased Pg
by 5.3 +/- 1.2 mmHg. Postglomerular resistance increased by 51% while
preglomerular resistance was unchanged in response to ANG II infusion
in dogs with intrarenal NO synthesis and voltage-gated calcium
channel blockade. These data indicate that the preglomerular response
to ANG II under conditions of reduced NO synthesis within the kidney
is dependent upon voltage-gated calcium channels.
Received 11 March 1996; accepted in final form 6 November 1996.
APS Manuscript Number R151-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996