RESUMO
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.
Assuntos
Coração/fisiopatologia , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Receptores de Droga/fisiologia , Animais , Antiarrítmicos/farmacologia , Antiarrítmicos/uso terapêutico , Canabinoides/farmacologia , Canabinoides/uso terapêutico , Doença das Coronárias/fisiopatologia , Dronabinol/análogos & derivados , Dronabinol/farmacologia , Dronabinol/uso terapêutico , Reperfusão Miocárdica , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Ratos , Ratos Wistar , Receptores de Canabinoides , Receptores de Droga/agonistasRESUMO
Intravenous injection of 10 mg/kg anandamide reduces the incidence and duration of epinephrine-induced arrhythmias in rats. SR141716A and SR144528, antagonists of cannabinoid receptor I and II did not abolish the antiarrhythmic effect of anandamide. These data suggest that the antiarrhythmic effect of anandamide is nonspecific or mediated via unknown cannabinoid receptors, but not associated with activation of cannabinoid receptors I and II.
