Vagally‐mediated gastrointestinal reflexes are modulated by central glucose levels

Abstract

The vagally‐mediated receptive relaxation reflex is activated upon distension of the esophagus and induces gastric relaxation and delays gastric emptying. Many gastrointestinal (GI) hormones exert dramatic control over vagally‐mediated GI functions via brainstem sites of action. The aim of this study was to determine whether glucose‐induced alterations in GI reflexes are achieved, in part, by brainstem sites of action.A balloon was used to distend the esophagus of adult rats and the resulting gastric relaxation measured via miniature strain gauges affixed to the stomach. Increasing blood glucose levels decreased the magnitude of the receptive relaxation from 0.6±0.1g to 0.4±0.1g and 0.3±0.1g at 3±0.2mM glucose, 6±0.5 and 10±1.8mM blood glucose, respectively (n=3). Similarly, altering brainstem glucose directly (via 4th ventricular application 3, 4.5 or 10mM glucose) decreased the receptive relaxation by 5±3, 15±0 and 20±3%, respectively (n=3). The glucose‐induced decreased receptive relaxation was blocked by brainstem application of the 5‐HT3 antagonist, ondansetron (30nmoles; 15±0.3% reduction to 10mM glucose vs 0±0.1% reduction in the presence of ondansetron, n=3).These results suggest that alterations in brainstem glucose levels, either directly or indirectly, exerts profound effects upon vagally‐mediated GI reflexes possibly via mechanism involving alterations in brainstem 5‐HT3 levelsSupported by DK 55530