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

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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

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ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)

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