Arginine vasopressin interacts with thromboxane in
hydronephrosis.
Takenaka, Tsuneo, and Hayley Forster.
Shinjuku Suimei Clinic, Tokyo, 160 Japan, and Miami VA Medical
Center and the University of Miami, Florida 33125 USA
APStracts 3:0185F, 1996.
The influence of hydronephrosis (6-10 weeks) on the renal vascular
response to arginine vasopressin (AVP) was assessed, using isolated
perfused normal and hydronephrotic rat kidneys. In normal kidneys,
AVP (0.3 nM) reduced renal perfusate flow (RPF) by 55 +/- 7 %
(p<0.01). AVP-induced decrements in RPF were reversed
partially by diltiazem (10 [mu]M) and completely by 10 nM of AVP (V1)
receptor antagonist (AVPX). In hydronephrotic kidneys, AVP reduced
RPF by 81 +/- 2 % (P<0.01) and constricted afferent (AA) and
efferent arterioles (EA) by 33 +/- 3 (P<0.01) and 33 +/- 5 %
(P<0.01), respectively. The addition of diltiazem altered
neither RPF nor vessel diameters. Administration of AVPX recovered
RPF, AA and EA diameters. When hydronephrotic kidneys were pretreated
with thromboxane (TBX) inhibitors, AVP reduced RPF by 62 +/- 5 %
(P<0.01) and constricted AAs and EAs by 26 +/- 2
(P<0.01) and 17 +/- 3 % (p<0.05), respectively. Under
TBX blockade, diltiazem partially reversed the AVP-induced reduction
in RPF and restored the decrements in AA diameter. Subsequent
addition of AVPX returned RPF and EA diameter. Our data indicate that
AVP elicits substantial renal microvascular constriction, and suggest
that AVP stimulates TBX production in hydronephrotic kidneys, thereby
altering renal vascular responsiveness to this peptide.
Received 30 October 1995; accepted in final form 16 September
1996.
APS Manuscript Number F370-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996