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Prevention by an inhibitor of the l ‐arginine‐nitric oxide pathway of the antiarrhythmic effects of bradykinin in anaesthetized dogs
Author(s) -
Vegh Agnes,
Papp Julius Gy,
Szekeres Laszlo,
Parratt James R.
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13764.x
Subject(s) - bradykinin , nitric oxide , pharmacology , arginine , anesthesia , medicine , nitric oxide synthase , bradykinin receptor , chloralose , chemistry , blood pressure , receptor , biochemistry , amino acid
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.