We conducted this study to identify the endocrine and neurocrine mechanisms of gastric mucosal protection in rats with experimental atrophic gastritis (erosive atrophic antritis) induced by prolonged exposure to taurocholate. This resulting gastritis was characterized by a significant reduction of parietal cell mass, a decrease in mucosal thickness, decreased numbers of pyloric glands, infiltration by inflammatory cells, and fibrotic proliferation in the gastric mucosa. Mucosal erosions were also prominent. These morphologic and morphometric findings indicate the presence of erosive atrophic gastritis, as previously described. Fasting levels of serum gastrin increased significantly in the rats with gastritis versus controls, whereas the mucosal gastrin levels did not differ significantly from those of controls. Mucosal levels of somatostatin decreased significantly, and vasoactive intestinal peptide (VIP) increased significantly in the pyloric sphincter region. These findings suggest that these peptides and neuropeptides are involved in the induction of this form of gastritis. The peptides may play an important role in the mechanisms of gastric mucosal protection (i.e., gastrin is an aggressive and somatostatin is a defensive factor, and VIP promotes the reflux of bile into the stomach by relaxing the pyloric sphincter).