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). Glibenclamide inhibited 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.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine