Stimuliatsiia del'ta1 opioidnykh retseptorov povyshaet porog zheludochkovoi fibrilliatsii pri postinfarktnom kardioskleroze: rol' K(ATP)-kanalov.

Translated title of the contribution: Stimulation of delta1-opioid receptors increases the ventricular fibrillation threshold in post-infarct cardiosclerosis: the role of K(ATP)-channels

N. V. Solenkova, L. N. Maslov, Yury Borisovich Lishmanov, V. I. Serebrov, S. A. Bogomaz, G. G. Gross, J. B. Stefano, S. V. Tam

Research output: Contribution to journalArticle

2 Citations (Scopus)


Preliminary administration of the delta 1-opioid receptor (delta 1-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 delta 1-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 delta 1-OR mediated increase in the VFT protective effect of the delta 1-OR stimulation. The intravenous injection of the mitochondrial KATP channel blocker 5-hydroxydecanoate (5 mg/kg) simultaneously with DPDPE not only eliminated the delta 1-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 delta 1-OR increases VFT by activating mitochondrial KATP-channels.

Original languageRussian
Pages (from-to)30-33
Number of pages4
JournalEksperimental'naya i Klinicheskaya Farmakologiya
Issue number1
Publication statusPublished - Jan 2002
Externally publishedYes


ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)

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