ATP-SENSITIVE K+ CHANNELS MEDIATE DILATATION OF CEREBRAL ARTERIOLES DURING HYPOXIA

We tested the hypothesis that dilatation of cerebral arterioles during hypoxia is mediated by activation of ATP-sensitive K+ channels. The diameter of pial arterioles was measured through a closed cranial window in anesthetized rabbits. Topical application of aprikalim (10(-6) mol/L), a direct activator of ATP-sensitive K+ channels, dilated pial arterioles by 18+/-3% (mean+/-SEM). Glibenclamide (10(-6) mol/L), an inhibitor of ATP-sensitive K+ channels, virtually abolished aprikalim-induced vasodilatation. When arterial PO2 was reduced from 129+/-3 to 25+/-1 mm Hg, the diameter of cerebral arterioles increased by 66+/-9% (P<.05). Glibendamide inhib-ited dilatation of pial arterioles during hypoxia by 46+/-5% (P<.05). In contrast, vasodilatation in response to sodium nitroprusside was not altered by glibenclamide. Topical application of adenosine (10(-4) mol/L) increased arteriolar diameter by 21+/-4%. Glibenclamide did not affect adenosine-induced vasodilatation. These findings suggest that dilatation of cerebral arterioles in response to hypoxia is mediated, in part, by activation of ATP-sensitive K+ channels.