ATP-sensitive K+ channel opener pinacidil augments β1-adrenoceptor-induced coronary vasodilation in dogs

Yousuke Katsuda, Kensuke Egashira, Hideki Ueno, Yukjnori Arai, Yutaka Akatsuka, Takeshi Kuga, Hiroaki Shimokawa, Akira Takeshita

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


The opening of ATP-sensitive K+ (KATP+) channels contributes to the mechanism of metabolic coronary vasodilation. The aim of the present study was to determine whether KATP+ channel opener pinacidil augments coronary vasodilation induced by β-adrenoceptor stimulation. In anesthetized dogs, coronary vasodilation in response to intracoronary infusion of a β1-adrenoceptor agonist denopamine, selective β2-adrenoceptor stimulation with isoproterenol after bisoprolol or nitroglycerin was studied before and during simultaneous intracoronary infusion of pinacidil at a dose of 1 μg/min, which had no effect on basal hemodynamics. Pinacidil augmented the denopamine-induced increase in coronary blood flow (CBF) from 38 ± 9 to 66 ± 16% (P < 0.05) but did not affect the denopamine-induced increase in myocardial oxygen consumption (MVo2). Pinacidil had no effect on the increases in CBF or MVo2 induced by isoproterenol or nitroglycerin. Thus pinacidil selectively augmented β1-adrenoceptor-mediated coronary vasodilation. These observations suggest that the KATP+ channel opener pinacidil may increase myocardial perfusion during metabolic stress associated with β1-adrenoceptor stimulation.

Original languageEnglish
JournalAmerican Journal of Physiology
Issue number6 PART 2
Publication statusPublished - 1996 Dec 1
Externally publishedYes


  • Coronary circulation
  • Metabolic coronary vasodilation

ASJC Scopus subject areas

  • Physiology (medical)


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