GLIBENCLAMIDE DOES NOT REVERSE ATTENUATED VASOREACTIVITY TO ACUTE OR CHRONIC HYPOXIA

Recent studies from our laboratory have shown that acute and chronic h ypoxic exposures are associated with attenuated systemic vasoreactivit y in conscious rats. The present studies examined the role of adenosin e triphosphate-sensitive potassium channels (K-ATP channels) in modula ting the presser and vasoconstrictor responses to phenylephrine (PE) i n conscious instrumented rats 1) during acute hypoxia or 2) after chro nic hypoxic exposure. Mean arterial. pressure, mean cardiac output, an d total peripheral resistance were assessed before and after graded in fusions of PE in both groups of rats under normoxic or hypoxic conditi ons. Additionally, the role of K-ATP channels in attenuating vasoreact ivity 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 animal s. Furthermore, acute return to room air did not restore the presser a nd constrictor responses in the chronically hypoxic rats. Glibenclamid e infusion did not influence the presser or vasoconstrictor responses to PE in either group of animals during normoxia or acute hypoxia. The refore, our data suggest that opening of K-ATP channels is not involve d in the attenuated vasoreactivity associated with acute and chronic h ypoxia in the conscious rat.