The effect of Katp channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis

N. V. Solenkova, L. N. Maslov, Vladimir Yurievich Serebrov, Yury Borisovich Lishmanov, S. A. Bogomaz, G. J. Gross, G. J. Grover

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Opening of the ATP-dependent K-channels (KATP channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective KATP channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial KATP channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoKATP channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoKATP channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoKATP channels increases the cardiac electrical stability in rats with PIC.

Original languageEnglish
Pages (from-to)10-13
Number of pages4
JournalEksperimental'naya i Klinicheskaya Farmakologiya
Volume67
Issue number3
Publication statusPublished - 2004
Externally publishedYes

Fingerprint

Rats
Myocardium
Ventricular Fibrillation
Chemical activation
KATP Channels
Diazoxide
Guanethidine
Glyburide
Intravenous Administration
Animals
Adenosine Triphosphate
Injections
BMS 180448
mitochondrial K(ATP) channel
Therapeutics

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

The effect of Katp channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis. / Solenkova, N. V.; Maslov, L. N.; Serebrov, Vladimir Yurievich; Lishmanov, Yury Borisovich; Bogomaz, S. A.; Gross, G. J.; Grover, G. J.

In: Eksperimental'naya i Klinicheskaya Farmakologiya, Vol. 67, No. 3, 2004, p. 10-13.

Research output: Contribution to journalArticle

@article{2cf4a2e64d8e49698b0214c3d2cc6765,
title = "The effect of Katp channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis",
abstract = "Opening of the ATP-dependent K-channels (KATP channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective KATP channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial KATP channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoKATP channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoKATP channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoKATP channels increases the cardiac electrical stability in rats with PIC.",
author = "Solenkova, {N. V.} and Maslov, {L. N.} and Serebrov, {Vladimir Yurievich} and Lishmanov, {Yury Borisovich} and Bogomaz, {S. A.} and Gross, {G. J.} and Grover, {G. J.}",
year = "2004",
language = "English",
volume = "67",
pages = "10--13",
journal = "Eksperimental'naya i Klinicheskaya Farmakologiya",
issn = "0869-2092",
publisher = "Izdatelstvo Meditsina",
number = "3",

}

TY - JOUR

T1 - The effect of Katp channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis

AU - Solenkova, N. V.

AU - Maslov, L. N.

AU - Serebrov, Vladimir Yurievich

AU - Lishmanov, Yury Borisovich

AU - Bogomaz, S. A.

AU - Gross, G. J.

AU - Grover, G. J.

PY - 2004

Y1 - 2004

N2 - Opening of the ATP-dependent K-channels (KATP channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective KATP channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial KATP channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoKATP channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoKATP channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoKATP channels increases the cardiac electrical stability in rats with PIC.

AB - Opening of the ATP-dependent K-channels (KATP channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective KATP channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial KATP channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoKATP channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoKATP channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoKATP channels increases the cardiac electrical stability in rats with PIC.

UR - http://www.scopus.com/inward/record.url?scp=3142676341&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3142676341&partnerID=8YFLogxK

M3 - Article

VL - 67

SP - 10

EP - 13

JO - Eksperimental'naya i Klinicheskaya Farmakologiya

JF - Eksperimental'naya i Klinicheskaya Farmakologiya

SN - 0869-2092

IS - 3

ER -