Atp- sensitive k+ channel opener pinacidil augments [beta]1
-adrenoceptor-induced coronary vasodilation in dogs.
Katsuda, Yousuke, Kensuke Egashira, Hideki Ueno, Yukinori Arai, Yutaka
Akatsuka, Takeshi Kuga, Hiroaki Shimokawa, Akira Takeshita.
The Research Institute of Angiocardiology and Cardiovascular
Clinic, Kyushu University School of Medicine, Fukuoka, Japan
APStracts 2:0571H, 1995.
The opening of ATP-sensitive K+ (K+ATP) channels contribute to the
mechanism of metabolic coronary vasodilation. The aim of the present
study was to determine whether a K+ATP channel opener pinacidil
augments coronary vasodilation induced by [beta]-adrenoceptor
stimulation. In anesthetized dogs, coronary vasodilation in response
to intracoronary infusion of a [beta]1-adrenoceptor agonist
denopamine, a selective [beta]2-adrenoceptor stimulation with
isoproterenol after bisoprolol, or nitroglycerin was studied before
and during simultaneous intracoronary infusion of pinacidil at a dose
of 1 [mu]g/min that 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 myocardial oxygen consumption (MVO2).
Pinacidil had no effect on the increases in CBF or MVO2 induced by
isoproterenol or by nitroglycerin. Thus, pinacidil selectively
augmented the [beta]1 adrenoceptor-mediated coronary vasodilation.
These observations suggest that the K+ATP channel opener pinacidil
may increase myocardial perfusion during metabolic stress associated
with [beta]1-adrenoceptor stimulation.
Received 2 August 1995; accepted in final form 11 December 1995.
APS Manuscript Number H728-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95