bq-485 and Stomach-Ulcer

Ammonia, one of the pathogenic factors in Helicobacter pylori-induced mucosal injury, induces acute mucosal lesions in the rat glandular stomach.. The effect of ammonia administered intragastrically on gastric peptides was investigated in urethane-anesthetized rats.. Gastric mucosal lesions were observed 5 min after 0.3% ammonia (4 ml/kg, intragastrically). Immunoreactive endothelin-1 (ET-1) and immunoreactive thyrotropin-releasing hormone (TRH) concentrations in the gastric wall decreased significantly 2 min and 5 min after ammonia, respectively. A significant increase in gastric juice immunoreactive ET-1 and TRH levels was reciprocally observed. The severity of gastric mucosal injury and changes in gastric immunoreactive ET-1 and TRH concentrations were shown to be concentration-dependent 30 min after ammonia. Atropine (5 mg/kg, intraperitoneally, -20 min) prevented ammonia-induced injury accompanied by a block of changes in gastric immunoreactive ET-1 and TRH concentrations. BQ-485 (ET(A) receptor antagonist; 2 mg/kg, subcutaneously) also abolished ammonia-induced lesions and gastric immunoreactive TRH changes.. These findings suggested that gastric ET-1 and TRH play a role in ammonia-induced gastric mucosal injury mediated via a muscarine and an ET(A) receptor.

Topics: Ammonia; Animals; Anti-Ulcer Agents; Atropine; Azepines; Dose-Response Relationship, Drug; Endothelin Receptor Antagonists; Endothelin-1; Gastric Juice; Gastric Mucosa; Male; Muscarinic Antagonists; Oligopeptides; Rats; Rats, Wistar; Somatostatin; Stomach Ulcer; Thyrotropin-Releasing Hormone; Time Factors