BRADYKININ, CORONARY-ARTERY DISEASE AND GASTROESOPHAGEAL REFLUX

Gastro-oesophageal reflux and coronary artery disease frequently of my ocardial vagal receptors oesophageal sphincter (LOS) function and may explain this link. This study examined the role of bradykinin, produce d in increased quantities by the ischaemic myocardium, in activating t his reflex. Thirteen dogs had patches soaked in bradykinin 100 mu g/ml and saline applied sequentially to the left ventricular epicardium. E leven of these animals were further divided into two subgroups: group 1 animals (six dogs) had the above sequence repeated after obliteratio n of sympathetic afferent fibres with phenol and those in group 2 (fiv e animals) underwent sequential intravenous and intra-atrial injection of bradykinin 0.2 mu g/kg. Epicardial bradykinin produced a fall in m ean(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 f rom 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 transi ent LOS relaxation, predisposing to gastro-oesophageal reflux.