Glibenclamide does not reverse attenuated vasoreactivity to acute
or chronic hypoxia.
Eichinger, Mark R., Thomas C. Resta, Dana S. Balderrama, Gerald M.
Herrera, Lidia A. Richardson, Juanita M. Resta, and Benjimen R.
Walker.
Department of Physiology, University of New Mexico School of
Medicine, Albuquerque, NM 87131
APStracts 2:0216A, 1995.
Recent studies from our laboratory have shown that acute and chronic
hypoxic exposure are associated with attenuated systemic
vasoreactivity in conscious rats. The present studies examined the
role of adenosine triphosphate sensitive potassium channels (KATP
channels) in modulating the pressor and vasoconstrictor responses to
phenylephrine (PE) in conscious, instrumented rats 1) during acute
hypoxia or 2) following chronic hypoxic exposure. Mean arterial
pressure (MABP), mean cardiac output (CO) and total peripheral
resistance (TPR) were assessed before and after graded infusions of
PE in both groups of rats under normoxic or hypoxic conditions.
Additionally, the role of KATP channels in attenuating vasoreactivity
was determined by administration of glibenclamide (KATP channel
blocker) prior to PE infusions. Acute hypoxia (12% 02) was associated
with reduced pressor and constrictor responses to PE in control
animals. Further, acute return to room-air did not restore the
pressor and constrictor responses in the chronically hypoxic (CH)
rats. Glibenclamide infusion did not influence the pressor or
vasoconstrictor responses to PE in either group of animals during
normoxia or acute hypoxia. Therefore, our data suggest that opening
of KATP channels is not involved in the attenuated vasoreactivity
associated with acute and chronic hypoxia in the conscious rat.
Received 8 February 1995; accepted in final form 15 May 1995.
APS Manuscript Number A149-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.