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

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    8 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)313-319
    Number of pages7
    JournalJournal of Cardiovascular Pharmacology
    Volume30
    Issue number3
    DOIs
    Publication statusPublished - 1997

    All Science Journal Classification (ASJC) codes

    • Pharmacology
    • Cardiology and Cardiovascular Medicine

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