[The role of opiate receptors and ATP-dependent potassium channels of mitochondria in the formation of myocardial adaptive resistance to the arrhythmogenic effect of ischemia and reperfusion]

Iu B Lishmanov; N V Naryzhnaia; A V Krylatov; L N Maslov; S A Bogomaz; D S Ugdyzhekova; G J Gross; J B Stefano

[The role of opiate receptors and ATP-dependent potassium channels of mitochondria in the formation of myocardial adaptive resistance to the arrhythmogenic effect of ischemia and reperfusion]

Izv Akad Nauk Ser Biol. 2003 Nov-Dec:(6):720-7.

[Article in Russian]

Authors

Iu B Lishmanov¹, N V Naryzhnaia, A V Krylatov, L N Maslov, S A Bogomaz, D S Ugdyzhekova, G J Gross, J B Stefano

Affiliation

¹ Institute of Cardiology, Tomsk Research Center, Siberian Division, Russian Academy of Medical Sciences, ul. Kievskaya 111a, Tomsk, 634050 Russia.

PMID: 14994477

Abstract

Preliminary stimulation of opiate receptors (ORs) by intravenous administration of mu agonist DALDA (0.5 mg/kg), delta 1 agonist DPDPE (0.5 mg/kg), and kappa agonist (-)-U-50.488 (1 mg/kg) increases rat myocardial resistance to arrhythmogenic effect of coronary occlusion (10 min) and reperfusion (10 min). Activation of delta 2 ORs (DSLET, 0.5 mg/kg) has no effect on the incidence rate of ischemic and reperfusion arrhythmias. Preliminary administration of glibenclamide (0.3 mg/kg), an inhibitor of KATP channels, blocks the antiarrhythmic effect of DALDA and DPDPE. Repeated short-term exposures of rats to immobilization within two weeks increases the heart tolerance to the arrhythmogenic effect of coronary occlusion and reperfusion. This effect disappears after administration of CTAP (0.5 mg/kg), a mu antagonist, or injection of 5-hydroxydecanoate (5 mg/kg), an inhibitor of mitochondrial KATP channels. The selective antagonists of delta and kappa ORs have no effect on cardiac adaptation-induced resistance to the arrhythmogenic effect of ischemia and reperfusion. We believe that stimulation of mu, delta, and kappa ORs increases myocardial tolerance to the arrhythmogenic effect of ischemia and reperfusion through activation of KATP channels. The antiarrhythmic effect of the adaptation is mediated by stimulation of mu ORs and mitochondrial KATP channels.

Publication types

English Abstract

MeSH terms

Adaptation, Physiological / drug effects
Adaptation, Physiological / physiology*
Adenosine Triphosphate / metabolism
Animals
Anti-Arrhythmia Agents / pharmacology
Arrhythmias, Cardiac / drug therapy
Arrhythmias, Cardiac / metabolism*
Coronary Disease
Decanoic Acids / pharmacology
Enkephalin, D-Penicillamine (2,5)- / pharmacology
Enkephalin, Leucine / analogs & derivatives*
Enkephalin, Leucine / pharmacology
Glyburide / pharmacology
Hydroxy Acids / pharmacology
Male
Mitochondria / drug effects
Mitochondria / metabolism
Myocardial Ischemia / complications
Myocardial Ischemia / drug therapy
Myocardial Ischemia / metabolism*
Myocardial Reperfusion / adverse effects
Myocardial Reperfusion Injury / complications
Myocardial Reperfusion Injury / drug therapy
Myocardial Reperfusion Injury / metabolism*
Narcotic Antagonists / pharmacology
Oligopeptides / pharmacology
Peptide Fragments
Peptides / pharmacology
Potassium Channels / metabolism*
Rats
Rats, Wistar
Receptors, Opioid / drug effects
Receptors, Opioid / metabolism*
Receptors, Opioid, delta / metabolism
Receptors, Opioid, mu / agonists
Receptors, Opioid, mu / antagonists & inhibitors
Receptors, Opioid, mu / metabolism
Somatostatin

Substances

Anti-Arrhythmia Agents
CTAP octapeptide
Decanoic Acids
Hydroxy Acids
Narcotic Antagonists
Oligopeptides
Peptide Fragments
Peptides
Potassium Channels
Receptors, Opioid
Receptors, Opioid, delta
Receptors, Opioid, mu
tyrosyl-arginyl-phenylalanyl-lysinamide
Somatostatin
Enkephalin, Leucine
5-hydroxydecanoic acid
enkephalin, Ser(2), Leu(5), Thr(6)-
Enkephalin, D-Penicillamine (2,5)-
Adenosine Triphosphate
Glyburide