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.
|Journal||American Journal of Physiology|
|Issue number||6 PART 2|
|Publication status||Published - 1996 Dec 1|
- Coronary circulation
- Metabolic coronary vasodilation
ASJC Scopus subject areas
- Physiology (medical)