GLIBENCLAMIDE DOES NOT REVERSE ATTENUATED VASOREACTIVITY TO ACUTE OR CHRONIC HYPOXIA

Recent studies from our laboratory have shown that acute and chronic hypoxic exposures are associated with attenuated systemic vasoreactivity in conscious rats. The present studies examined the role of adenosine triphosphate-sensitive potassium channels (K-ATP channels) in modulating the presser and vasoconstrictor responses to phenylephrine (PE) in conscious instrumented rats 1) during acute hypoxia or 2) after chronic hypoxic exposure. Mean arterial. pressure, mean cardiac output, and total peripheral resistance were assessed before and after graded infusions of PE in both groups of rats under normoxic or hypoxic conditions. Additionally, the role of K-ATP channels in attenuating vasoreactivity was determined by administration of glibenclamide (K-ATP channel blocker) before PE infusions. Acute hypoxia (12% O-2) was associated with reduced presser and constrictor responses to PE in control animals. Furthermore, acute return to room air did not restore the presser and constrictor responses in the chronically hypoxic rats. Glibenclamide infusion did not influence the presser or vasoconstrictor responses to PE in either group of animals during normoxia or acute hypoxia. Therefore, our data suggest that opening of K-ATP channels is not involved in the attenuated vasoreactivity associated with acute and chronic hypoxia in the conscious rat.