ATP-sensitive K+ channels mediate dilatation of cerebral arterioles during hypoxia

Hisao Taguchi, Donald D. Heistad, Takanari Kitazono, Frank M. Faraci

研究成果: ジャーナルへの寄稿学術誌査読

101 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)1005-1008
ページ数4
ジャーナルCirculation research
74
5
DOI
出版ステータス出版済み - 5月 1994
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 生理学
  • 循環器および心血管医学

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