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 language | English |
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Pages (from-to) | 523-525 |
Number of pages | 3 |
Journal | Bulletin of Experimental Biology and Medicine |
Volume | 131 |
Publication status | Published - 2001 |
Keywords
- arrhythmias
- cannabinoid receptors
- K+ channels
- VENTRICULAR ARRHYTHMIAS
- ISCHEMIA
- PHARMACOLOGY
- INFARCTION
- MECHANISMS
- RATS