Glibenclamide, a specific inhibitor of ATP-sensitive K+ channels, inhibits coronary vasodilation induced by angiotensin II-receptor antagonists

H. Tada, K. Egashira, M. Yamamoto, H. Ueno, M. Takemoto, H. Shimokawa, A. Takeshita

    研究成果: Contribution to journalArticle査読

    8 被引用数 (Scopus)

    抄録

    The purpose of our study was test the hypothesis that endogenous angiotensin II contributes to the basal coronary artery tone by acting at vascular ATP-sensitive K+ (K+ATP) channels. Coronary blood flow (CBF) and other hemodynamic parameters were measured in anesthetized dogs. Intracoronary infusion of the selective antagonists of angiotensin II AT1 receptors (L-158,809 and E4177) increased CBF without affecting other hemodynamic parameters, indicating that endogenous angiotensin II caused coronary vasoconstriction through the AT1 subtype receptors. Coronary vasodilation in response to AT1 receptor antagonists was blunted by pretreatment with glibenclamide (a specific inhibitor of K+ATP channels; p < 0.01) but not by either an adenosine-receptor antagonist or an inhibitor of nitric oxide synthesis. Coronary vasodilation in response to AT1-receptor antagonists was partly reduced (p < 0.01) by PD-123319 (the AT2-receptor antagonist). Glibenclamide had no effect on coronary vasodilation induced by sodium nitroprusside. These results indicate that in dogs in vivo, coronary vasodilation in response to AT1-receptor antagonists inhibited markedly by glibenclamide and partly by PD-123319, suggesting that endogenous angiotensin II contributes to the maintenance of basal coronary vascular tone by acting at K+ATP channels through its receptors.

    本文言語英語
    ページ(範囲)313-319
    ページ数7
    ジャーナルJournal of Cardiovascular Pharmacology
    30
    3
    DOI
    出版ステータス出版済み - 1997

    All Science Journal Classification (ASJC) codes

    • Pharmacology
    • Cardiology and Cardiovascular Medicine

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