Staunton, E.Smid, S.Dent, J.Blackshaw, L.2006-06-262006-06-262000American Journal of Physiology - Gastrointestinal and Liver Physiology, 2000; 279(1 42-1):G157-G1620193-18571522-1547http://hdl.handle.net/2440/9243Activation of gastric vagal mechanoreceptors by distention is thought to be the trigger for transient lower esophageal sphincter relaxations (TLESR), which lead to gastroesophageal reflux. The contribution of higher-threshold gastric splanchnic mechanoreceptors is uninvestigated. GABA(B) receptor agonists, including baclofen, potently reduce triggering of TLESR by low-level gastric distention. We aimed to determine first whether this effect of baclofen is maintained at high-level distention and second the role of splanchnic pathways in triggering TLESR. Micromanometric/pH studies in conscious ferrets showed that intragastric glucose infusion (25 ml) increased triggering of TLESR and reflux. Both were significantly reduced by baclofen (7 micromol/kg ip) (P < 0.05). When 40 ml of air was added to the glucose infusion, more TLESR occurred than with glucose alone (P < 0.01). These were also reduced by baclofen (P < 0.001). TLESR after glucose/air infusion were assessed before and after splanchnectomy (2-4, 9-11, and 23-25 days), which revealed no change. Baclofen inhibits TLESR after both low- and high-level gastric distention. Splanchnic pathways do not contribute to increased triggering of TLESR by high-level gastric distention.enMuscle, SmoothEsophagogastric JunctionSplanchnic NervesAnimalsFerretsGastroesophageal RefluxBaclofenCapsaicinGlucoseReceptors, GABA-BMuscle Relaxants, CentralMuscle DenervationEatingPressureFemaleJournal article000100207010.1152/ajpgi.2000.279.1.g1570000881447000192-s2.0-003385491062854Smid, S. [0000-0003-4192-7219]