TGF-β3 inhibits pentagastrin-stimulated gastric acid secretion in rats

Background: Transforming growth factor beta(3) (TGF-beta(3)) has been shown to accelerate gastric ulcer healing in rats. However, little is known about the mechanism. In this study we investigated the influence of TGF-beta(3) on gastric acid secretion, since gastric hyperacidity is a major cause of gastroduodenal ulcer disease. Material/Methods: Male Sprague Dawley rats were equipped with gastric Thomas cannulas and jugular vein catheters. The acute effect of either intravenous TGF-beta(3) (400 and 1200 mu g/kg/h) or saline (0.15 M) on pentagastrin-stimulated (10 mu g/kg/h) gastric acid secretion was evaluated by gastric acid back-titration after 5 days of recovery. Additionally, pentagastrin-stimulated gastric acid secretion was assessed after 48 hours following TGF-beta(3) (1200 mu g/kg/h) or saline treatment. Results: Pentagastrin significantly increased gastric acid production. TGF-beta(3) significantly reduced pentagastrin-stimulated gastric acid secretion in a dose-dependent manner as early as 15 minutes after application (saline: 124.9 +/- 14.9 mu Eq H-circle plus/15 min, TGF-beta(3): 97.7 +/- 13.1 9 mu q H-circle plus/15 min, p < 0.002). Additionally, pretreatment with TGF-beta(3) abolished the effect of pentagastrin on gastric acid production. This effect lasted throughout the entire recording period of 48 hours. However, baseline physiological gastric acid production was not altered by TGF-beta(3). Conclusions: TGF-beta(3) inhibits gastric acid secretion when given prior to as well as after pentagastrin treatment. This implicates both a preventive and a therapeutic role of TGF-beta(3) in gastroduodenal ulcer disease.