PREVENTION BY AN INHIBITOR OF THE L-ARGININE-NITRIC OXIDE PATHWAY OF THE ANTIARRHYTHMIC EFFECTS OF BRADYKININ IN ANESTHETIZED DOGS

The intracoronary administration of bradykinin (25 ng kg-1 min-1) markedly reduces the severity of arrhythmias that occur during a 25 min occlusion of the left anterior descending coronary artery in chloralose, urethane anaesthetized dogs. This protection was abolished by the prior administration, by the same route, of N(G)-nitro-L-arginine methyl ester (L-NAME); an inhibitor of the L-arginine-nitric oxide pathway. The protective effect of bradykinin on reperfusion-induced VF was not affected by L-NAME. These results strongly suggest that the antiarrhythmic effect of bradykinin in this model is mediated by nitric oxide release. It also supports the concept that bradykinin might be a 'primary mediator' of the protective antiarrhythmic effects of ischaemic preconditioning.