Activation of type II cannabinoid receptors improves myocardial tolerance to arrhythmogenic effects of coronary occlusion and reperfusion

A V Krylatov, D S Ugdyshekova, N A Bernatskaya, L N Maslov, R Mekhoulam, R G Pertwee, G B Stephano

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Abstract

Preliminary intravenous injection of cannabinoid receptor agonist HU-210 (0.05 mg/kg) reduced the incidence of ventricular arrhythmias during 10-min coronary occlusion and 10-min reperfusion in chloralose-anesthetized rats. Preliminary injection of type I cannabinoid receptor antagonist SR 141716A (3 mg/kg) had no effect on the antiarrhythmic effect of HU-210, while type II cannabinoid receptor antagonist SR 144528 (1 mg/kg) completely abolished the effect of HU-210. Preconditioning with glibenclamide (0.3 mg/kg), an inhibitor of ATP-dependent K+-channels, did not affect the antiarrhythmic activity of HU-210. These findings suggest that antiarrhythmic effect of HU-210 is mediated through activation of type II cannabinoid receptors rather than activation of K+-channels.

Original languageEnglish
Pages (from-to)523-525
Number of pages3
JournalBulletin of Experimental Biology and Medicine
Volume131
Publication statusPublished - 2001

Keywords

  • arrhythmias
  • cannabinoid receptors
  • K+ channels
  • VENTRICULAR ARRHYTHMIAS
  • ISCHEMIA
  • PHARMACOLOGY
  • INFARCTION
  • MECHANISMS
  • RATS

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