Effect of esophageal distension on gastric secretions in rat and the possible mechanism

Introduction: The effect of esophageal distension (ED) on gastric motility has been well documented, but a few investigations have been carried out on the effect of ED on gastric secretion. The aim of this study was to investigate the effect of ED on gastric acid and pepsin secretion and the mechanism(s) involved. Methods: Male adult Wistar rats (200-240 g) were anesthetized with urethane (1.2 g/kg, i.p.) and underwent tracheostomy and laparotomy. A catheter was inserted in the stomach through duodenum for gastric distension and gastric washout. Esophagus was distended by a balloon (0.3 ml, 10 min). Gastric acid secretion was stimulated by gastric distension (by saline 1.5 ml/100 g of B.W.), pentagastrin (20 μg/kg, i.p.) or insulin (0.6 IU/kg, i.p.). Pepsin secretion was stimulated by carbachol (20 μg/kg, i.p.). Effects of cervical vagotomy and reserpine (1 mg/kg, i.p.) were also investigated. Results: Gastric distension-, pentagastrin- and insulin-stimulated gastric acid secretion were decreased by esophageal distension (P<0.001, P<0.05 and P<0.05, respectively). Carbachol-induced pepsin secretion was also attenuated by esophageal distension (P<0.05). Cervical vagotomy abolished the inhibitory effect of ED on gastric distension-induced acid secretion. In reserpinized rats, ED reduced the basal gastric acid secretion (P<0.05). Conclusion: Results indicated that the ED decreased gastric acid output. The vagus nerve was involved in the inhibitory effect of the ED on gastric acid secretion but the adrenergic system did not play role.