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

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

Результат исследований: Материалы для журналаСтатья

2 Цитирования (Scopus)

Выдержка

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.

Язык оригиналаРусский
Страницы (с-по)30-33
Число страниц4
ЖурналEksperimental'naya i Klinicheskaya Farmakologiya
Том65
Номер выпуска1
СостояниеОпубликовано - янв 2002
Опубликовано для внешнего пользованияДа

Отпечаток

Opioid Receptors
Ventricular Fibrillation
delta Opioid Receptor
D-Penicillamine (2,5)-Enkephalin
Adenosine Triphosphate
Glyburide
KATP Channels
Narcotic Antagonists
Rats
Intravenous Injections
Peptides
mitochondrial K(ATP) channel

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)

Цитировать

Stimuliatsiia del'ta1 opioidnykh retseptorov povyshaet porog zheludochkovoi fibrilliatsii pri postinfarktnom kardioskleroze : rol' K(ATP)-kanalov. / Solenkova, N. V.; Maslov, L. N.; Lishmanov, Yury Borisovich; Serebrov, V. I.; Bogomaz, S. A.; Gross, G. G.; Stefano, J. B.; Tam, S. V.

В: Eksperimental'naya i Klinicheskaya Farmakologiya, Том 65, № 1, 01.2002, стр. 30-33.

Результат исследований: Материалы для журналаСтатья

@article{62692f7775694e69899948816b8addfe,
title = "Stimuliatsiia del'ta1 opioidnykh retseptorov povyshaet porog zheludochkovoi fibrilliatsii pri postinfarktnom kardioskleroze: rol' K(ATP)-kanalov.",
abstract = "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.",
author = "Solenkova, {N. V.} and Maslov, {L. N.} and Lishmanov, {Yury Borisovich} and Serebrov, {V. I.} and Bogomaz, {S. A.} and Gross, {G. G.} and Stefano, {J. B.} and Tam, {S. V.}",
year = "2002",
month = "1",
language = "Русский",
volume = "65",
pages = "30--33",
journal = "Eksperimental'naya i Klinicheskaya Farmakologiya",
issn = "0869-2092",
publisher = "Izdatelstvo Meditsina",
number = "1",

}

TY - JOUR

T1 - Stimuliatsiia del'ta1 opioidnykh retseptorov povyshaet porog zheludochkovoi fibrilliatsii pri postinfarktnom kardioskleroze

T2 - rol' K(ATP)-kanalov.

AU - Solenkova, N. V.

AU - Maslov, L. N.

AU - Lishmanov, Yury Borisovich

AU - Serebrov, V. I.

AU - Bogomaz, S. A.

AU - Gross, G. G.

AU - Stefano, J. B.

AU - Tam, S. V.

PY - 2002/1

Y1 - 2002/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0036372199&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036372199&partnerID=8YFLogxK

M3 - Статья

C2 - 12025781

AN - SCOPUS:0036372199

VL - 65

SP - 30

EP - 33

JO - Eksperimental'naya i Klinicheskaya Farmakologiya

JF - Eksperimental'naya i Klinicheskaya Farmakologiya

SN - 0869-2092

IS - 1

ER -