Y. Katsuda et al., ATP-SENSITIVE K-ADRENOCEPTOR-INDUCED CORONARY VASODILATION IN DOGS( CHANNEL OPENER PINACIDIL AUGMENTS BETA(1)), American journal of physiology. Heart and circulatory physiology, 39(6), 1996, pp. 2210-2215
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 augme
nts coronary vasodilation induced by beta-adrenoceptor stimulation. In
anesthetized dogs, coronary vasodilation in response to intracoronary
infusion of a beta(1)-adrenoceptor agonist denopamine, selective beta
(2)-adrenoceptor stimulation with isoproterenol after bisoprolol or ni
troglycerin was studied before and during simultaneous intracoronary i
nfusion of pinacidil at a dose of 1 mu g/min, which had no effect on b
asal hemodynamics. Pinacidil augmented the denopamine-induced increase
in coronary blood flow (CBF) from 38 +/- 9 to 66 +/- 16% (P < 0.05) b
ut did not affect the denopamine-induced increase in myocardial oxygen
consumption (MV(O)2). Pinacidil had no effect on the increases in CBF
or MV(O)2 induced by isoproterenol or nitroglycerin. Thus pinacidil s
electively augmented beta(1)-adrenoceptor-mediated coronary vasodilati
on. These observations suggest that the K-ATP(+) channel opener pinaci
dil may increase myocardial perfusion during metabolic stress associat
ed with beta(1)-adrenoceptor stimulation.