Myogenic contribution to agonist-induced renal vasoconstriction
during normoxia and hypoxia.
Eichinger, Mark R., Juanita M. Resta, and Benjimen R. Walker.
Department of Physiology, University of New Mexico, School of
Medicine, Albuquerque, NM 87131
APStracts 3:0481H, 1996.
Acute hypoxia attenuates agonist-induced constrictor and pressor
responses in conscious rats, and a recent report suggests that
hypoxia may also diminish myogenic reactivity in isolated, perfused
rat kidneys. Thus, we hypothesized that the diminished responsiveness
to pressor agents during hypoxia is due to an impairment of myogenic
reactivity. Male, Sprague-Dawley rats were instrumented with a pulsed
Doppler flow probe on the left renal artery, an aortic vascular
occluder cuff immediately above the left renal artery to control
renal perfusion pressure, and catheters to measure systemic arterial
blood pressure, renal artery pressure (RAP), and for administration
of agents. Animals were studied under normoxic or acute hypoxic
(FIO2=0.12) conditions and were administered phenylephrine, arginine
vasopressin, or angiotensin II. To determine the myogenic (pressure
-dependent) component of agonist-induced vasoconstriction, renal
vascular resistance (RVR) was calculated during agonist infusion with
RAP uncontrolled and with RAP controlled to preinfusion levels.
Significant myogenic components of agonist-induced renal
vasoconstriction were evident with all pressor agents employed.
However, hypoxia did not attenuate agonist-induced, pressure
-dependent increases in RVR. We conclude that the reduced
vasoreactivity associated with acute hypoxia is not due to diminished
myogenic reactivity.
Received 29 May 1996; accepted in final form 22 October 1996.
APS Manuscript Number H477-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996