Bradykinin, coronary artery disease and gastro-oesophageal reflux

Gastro‐oesophageal reflux and coronary artery disease frequently coexist. Stimulation of myocardial vagal receptors impairs lower oesophageal sphincter (LOS) function and may explain this link. This study examined the role of bradykinin, produced in increased quantities by the ischaemic myocardium, in activating this reflex. Thirteen dogs had patches soaked in bradykinin 100 μg/ml and saline applied sequentially to the left ventricular epicardium. Eleven of these animals were further divided into two subgroups: group 1 animals (six dogs) had the above sequence repeated after obliteration of sympathetic afferent fibres with phenol and those in group 2 (five animals) underwent sequential intravenous and intra‐atrial injection of bradykinin 0·2 μg/kg. Epicardial bradykinin produced a fall in mean(s.e.m.) LOS tone from 13·3(1·3) to 6·0(0·5) sphinctometer units (P< 0·002), accompanied by a reduction in mean(s.e.m.) arterial pressure from 95(4) to 83(5) mmHg (P< 0·002). Destruction of sympathetic afferent fibres did not alter the LOS effect. Intra‐atrial, but not intravenous, bradykinin reproduced the LOS effect. this suggests a cardiac origin. Myocardial release of bradykinin may play a role in producing transient LOS relaxation, predisposing to gastro‐oesophageal reflux.