Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, attenuates metabolic coronary vasodilatation induced by pacing tachycardia in dogs

Yousuke Katsuda, Kensuke Egashira, Hideki Ueno, Yutaka Akatsuka, Takahiro Narishige, Yukinori Arai, Tsuneo Takayanagi, Hiroaki Shimokawa, Akira Takeshita

Research output: Contribution to journalArticle

29 Citations (Scopus)

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 languageEnglish
Pages (from-to)511-517
Number of pages7
JournalCirculation
Volume92
Issue number3
DOIs
Publication statusPublished - Aug 1 1995

Fingerprint

Glyburide
Tachycardia
Vasodilation
Adenosine Triphosphate
Dogs
Pinacidil
Ventricular Pressure
Oxygen Consumption
Adrenergic Receptors
Blood Vessels
Arterial Pressure
Heart Rate

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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 journalArticle

Katsuda, Yousuke ; Egashira, Kensuke ; Ueno, Hideki ; Akatsuka, Yutaka ; Narishige, Takahiro ; Arai, Yukinori ; Takayanagi, Tsuneo ; Shimokawa, Hiroaki ; Takeshita, Akira. / Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, attenuates metabolic coronary vasodilatation induced by pacing tachycardia in dogs. In: Circulation. 1995 ; Vol. 92, No. 3. pp. 511-517.
@article{7148c4d60dba4e7fb05ad945a0c08b64,
title = "Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, attenuates metabolic coronary vasodilatation induced by pacing tachycardia in dogs",
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.",
author = "Yousuke Katsuda and Kensuke Egashira and Hideki Ueno and Yutaka Akatsuka and Takahiro Narishige and Yukinori Arai and Tsuneo Takayanagi and Hiroaki Shimokawa and Akira Takeshita",
year = "1995",
month = "8",
day = "1",
doi = "10.1161/01.CIR.92.3.511",
language = "English",
volume = "92",
pages = "511--517",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

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.

UR - http://www.scopus.com/inward/record.url?scp=0029092970&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029092970&partnerID=8YFLogxK

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 -