TY - JOUR
T1 - ATP-sensitive K+ channel opener pinacidil augments β1-adrenoceptor- induced coronary vasodilation in dogs
AU - Katsuda, Yousuke
AU - Egashira, Kensuke
AU - Ueno, Hideki
AU - Arai, Yukinori
AU - Akatsuka, Yutaka
AU - Kuga, Takeshi
AU - Shimokawa, Hiroaki
AU - Takeshita, Akira
PY - 1996/6
Y1 - 1996/6
N2 - 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.
AB - 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.
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U2 - 10.1152/ajpheart.1996.270.6.h2210
DO - 10.1152/ajpheart.1996.270.6.h2210
M3 - Article
C2 - 8764276
AN - SCOPUS:0029760570
SN - 0363-6135
VL - 270
SP - H2210-H2215
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 6 39-6
ER -