Background: The effect of esophageal distention (ED) on gastric motility has been well documented, but only a few investigations have been carried out about the effect of ED on gastric secretions. The aim of this study was to investigate the effect of ED on gastric acid and pepsin secretions and the mechanisms involved.
Methods: Male adult Wistar rats (200-240 g) were anesthetized by urethane [1.2 g/kg, intraperitoneally (i.p.)] and underwent tracheostomy and laparotomy. A catheter was inserted in the stomach through the duodenum for gastric washout and distention followed by the esophageal distention by a balloon (0.3 ml, 10 min). Gastric acid secretion was stimulated by gastric distension (1.5 ml/100 g body weight), pentagastrin (20 microg/kg, i.p.), or insulin (0.6 IU/kg, i.p.). Pepsin secretion was stimulated by carbachol (20 microg/kg, i.p.). Effects of cervical vagotomy and reserpine (1 mg/kg, i.p.) were also investigated.
Results: Gastric distention-, pentagastrin-, and insulin-stimulated gastric acid secretion was reduced by esophageal distention (P < 0.001, P < 0.05, and P < 0.05, respectively). Carbachol-induced pepsin secretion was also attenuated by esophageal distention (P < 0.05). Cervical vagotomy abolished the inhibitory effect of ED on pentagastrin-induced gastric acid secretion. In reserpinized rats, ED reduced the basal gastric acid secretion (P < 0.05).
Conclusions: These results indicate that the vagus nerves are involved in the inhibitory effect of esophageal distension on gastric secretory function.