Stimulation of δ1-opioid receptors increases the threshold for ventricular fibrillation in postinfarction cardiosclerosis

The role of KATP channels

N. V. Solenkova, L. N. Maslov, Yu B. Lishmanov, Vladimir Yurievich Serebrov, S. A. Bogomaz, G. G. Gross, J. B. Stefano, S. W. Tam

Research output: Contribution to journalArticle

Abstract

Preliminary administration of the δ1-opioid receptor (δ1-OR) selective peptide agonist DPDPE (0.1 mg/kg, i.v.) increased the ventricular fibrillation threshold (VFT) in postinfarction cardiosclerosis in rats. Pretreatment with the selective δ1-OR antagonists ICI 174,864 (not affecting VFT) in a dose of 0.5 mg/kg completely eliminated the DPDPE-induced increase in the VFT. Pretreatment with the KATP channel selective blocker glibenclamide (0.3 mg/kg, i.v.) completely eliminated the δ1-OR mediated increase in the VFT protective effect of the δ1-OR stimulation. The intravenous injection of the mitochondrial KATP channel blocker 5-hydroxydecanoate (5 mg/kg) simultaneously with DPDPE not only eliminated the δ1-OR mediated increase on VFT, but additionally increased the VBFT drop caused by cardiosclerosis. Injected separately, neither glibenclamide nor hydroxydecanoate affected the VFT level. It is concluded that stimulation of the δ1-OR increases VFT by activating mitochondrial KATP-channels.

Original languageEnglish
Pages (from-to)33
Number of pages1
JournalEksperimental'naya i Klinicheskaya Farmakologiya
Volume65
Issue number1
Publication statusPublished - 2002

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KATP Channels
Opioid Receptors
Ventricular Fibrillation
D-Penicillamine (2,5)-Enkephalin
Glyburide
Narcotic Antagonists
Rats
Intravenous Injections
Peptides

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)

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Stimulation of δ1-opioid receptors increases the threshold for ventricular fibrillation in postinfarction cardiosclerosis : The role of KATP channels. / Solenkova, N. V.; Maslov, L. N.; Lishmanov, Yu B.; Serebrov, Vladimir Yurievich; Bogomaz, S. A.; Gross, G. G.; Stefano, J. B.; Tam, S. W.

In: Eksperimental'naya i Klinicheskaya Farmakologiya, Vol. 65, No. 1, 2002, p. 33.

Research output: Contribution to journalArticle

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