Abstract
Background: We previously reported that glibenclamide (a selective inhibitor of ATP-sensitive K+ channels [K+(ATP) channels) inhibited metabolic coronary vasodilatation induced by β1-adrenoceptor stimulation. However, the role of K+(ATP) channels in metabolic coronary vasodilatation induced by tachycardia is still unknown. This study aimed to determine whether glibenclamide attenuates metabolic coronary vasodilatation induced by pacing-induced tachycardia. Methods and Results: In anesthetized dogs, increasing heart rate from 103±1 to 160 beats per minute with atrial pacing increased coronary blood flow without altering arterial pressure and left ventricular pressure. Intracoronary infusion of glibenclamide at 1.5 and 5.0 μg · kg-1 · min-1 did not alter basal coronary blood flow but significantly attenuated (P<.01) the tachycardia-induced coronary vasodilatation without altering the tachycardia-induced increase in myocardial oxygen consumption (MV̇O2). In conscious dogs, intracoronary glibenclamide at 5.0 μg · kg-1 · min-1 attenuated (P<.05) coronary vasodilatation induced by ventricular pacing from 85±6 to 150 beats per minute. Glibenclamide markedly attenuated coronary vasodilatation evoked with the K+(ATP) channel opener pinacidil. Conclusions: These data indicate that blockade of coronary vascular K+(ATP) channels with glibenclamide inhibited metabolic coronary vasodilatation induced by pacing tachycardia in dogs, suggesting that K+(ATP) channels are involved in the mechanism mediating metabolic coronary vasodilatation associated with pacing tachycardia.
| Original language | English |
|---|---|
| Pages (from-to) | 511-517 |
| Number of pages | 7 |
| Journal | Circulation |
| Volume | 92 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Aug 1 1995 |
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All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)
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Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, attenuates metabolic coronary vasodilatation induced by pacing tachycardia in dogs. / Katsuda, Yousuke; Egashira, Kensuke; Ueno, Hideki; Akatsuka, Yutaka; Narishige, Takahiro; Arai, Yukinori; Takayanagi, Tsuneo; Shimokawa, Hiroaki; Takeshita, Akira.
In: Circulation, Vol. 92, No. 3, 01.08.1995, p. 511-517.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, attenuates metabolic coronary vasodilatation induced by pacing tachycardia in dogs
AU - Katsuda, Yousuke
AU - Egashira, Kensuke
AU - Ueno, Hideki
AU - Akatsuka, Yutaka
AU - Narishige, Takahiro
AU - Arai, Yukinori
AU - Takayanagi, Tsuneo
AU - Shimokawa, Hiroaki
AU - Takeshita, Akira
PY - 1995/8/1
Y1 - 1995/8/1
N2 - Background: We previously reported that glibenclamide (a selective inhibitor of ATP-sensitive K+ channels [K+(ATP) channels) inhibited metabolic coronary vasodilatation induced by β1-adrenoceptor stimulation. However, the role of K+(ATP) channels in metabolic coronary vasodilatation induced by tachycardia is still unknown. This study aimed to determine whether glibenclamide attenuates metabolic coronary vasodilatation induced by pacing-induced tachycardia. Methods and Results: In anesthetized dogs, increasing heart rate from 103±1 to 160 beats per minute with atrial pacing increased coronary blood flow without altering arterial pressure and left ventricular pressure. Intracoronary infusion of glibenclamide at 1.5 and 5.0 μg · kg-1 · min-1 did not alter basal coronary blood flow but significantly attenuated (P<.01) the tachycardia-induced coronary vasodilatation without altering the tachycardia-induced increase in myocardial oxygen consumption (MV̇O2). In conscious dogs, intracoronary glibenclamide at 5.0 μg · kg-1 · min-1 attenuated (P<.05) coronary vasodilatation induced by ventricular pacing from 85±6 to 150 beats per minute. Glibenclamide markedly attenuated coronary vasodilatation evoked with the K+(ATP) channel opener pinacidil. Conclusions: These data indicate that blockade of coronary vascular K+(ATP) channels with glibenclamide inhibited metabolic coronary vasodilatation induced by pacing tachycardia in dogs, suggesting that K+(ATP) channels are involved in the mechanism mediating metabolic coronary vasodilatation associated with pacing tachycardia.
AB - Background: We previously reported that glibenclamide (a selective inhibitor of ATP-sensitive K+ channels [K+(ATP) channels) inhibited metabolic coronary vasodilatation induced by β1-adrenoceptor stimulation. However, the role of K+(ATP) channels in metabolic coronary vasodilatation induced by tachycardia is still unknown. This study aimed to determine whether glibenclamide attenuates metabolic coronary vasodilatation induced by pacing-induced tachycardia. Methods and Results: In anesthetized dogs, increasing heart rate from 103±1 to 160 beats per minute with atrial pacing increased coronary blood flow without altering arterial pressure and left ventricular pressure. Intracoronary infusion of glibenclamide at 1.5 and 5.0 μg · kg-1 · min-1 did not alter basal coronary blood flow but significantly attenuated (P<.01) the tachycardia-induced coronary vasodilatation without altering the tachycardia-induced increase in myocardial oxygen consumption (MV̇O2). In conscious dogs, intracoronary glibenclamide at 5.0 μg · kg-1 · min-1 attenuated (P<.05) coronary vasodilatation induced by ventricular pacing from 85±6 to 150 beats per minute. Glibenclamide markedly attenuated coronary vasodilatation evoked with the K+(ATP) channel opener pinacidil. Conclusions: These data indicate that blockade of coronary vascular K+(ATP) channels with glibenclamide inhibited metabolic coronary vasodilatation induced by pacing tachycardia in dogs, suggesting that K+(ATP) channels are involved in the mechanism mediating metabolic coronary vasodilatation associated with pacing tachycardia.
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U2 - 10.1161/01.CIR.92.3.511
DO - 10.1161/01.CIR.92.3.511
M3 - Article
VL - 92
SP - 511
EP - 517
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 3
ER -