The opening of ATP-sensitive K+ (K(ATP)/+) channels contributes to the mechanism of metabolic coronary vasodilation. The aim of the present study was to determine whether K(ATP)/+ 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 (MV̇O2). Pinacidil had no effect on the increases in CBF or MV̇O2 induced by isoproterenol or nitroglycerin. Thus pinacidil selectively augmented β1-adrenoceptor-mediated coronary vasodilation. These observations suggest that the K(ATP)/+ channel opener pinacidil may increase myocardial perfusion during metabolic stress associated with β1-adrenoceptor stimulation.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||6 39-6|
|Publication status||Published - Jun 1996|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)