Prevention by an inhibitor of the l‐arginine‐nitric oxide pathway of the antiarrhythmic effects of bradykinin in anaesthetized dogs

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Abstract
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 NG-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.