Helicobacter pylori and gastric acid overproduction are involved in peptic ulcer. H. pylori may increase or inhibit acid secretion depending on the effect of hormones and cytokines on parietal cells and the duration of gastritis. We studied acid variations in cats harboring Helicobacter felis, H. pylori, or free of gastric pathogens. Methods. Basal and stimulated gastric secretions, and plasma gastrin levels were determined in nine cats. Gastric biopsies were collected for histology before each experiment. We analyzed the effects of thioperamide, an H3-receptor antagonist, and SR27417A, a PAF-receptor antagonist, on stimulated acid secretion. Results. In cats harboring H. felis, gastric mucosa were histologically normal . After H. felis eradication, pentagastrin-stimulated acid secretion was increased by 40% compared to the situation before eradication. Thioperamide abolished the inhibitory effects of H. felis on acid secretion whereas SR27417A did not. Basal and meal-stimulated plasma gastrin levels were not affected by eradication therapy. Cats were then infected with H. pylori: acid secretion was inhibited by 80% in the 3^rd week and increased from the 5^th to the 7^th week, reaching the level in uninfected animals by the 9^th week and remained constant for up to 42 weeks after H. pylori infection. Thioperamide increased acid secretion by 20% in the 3^rd and 7^th weeks but acid levels were similar thereafter in untreated and treated cats. SR47217A had no effect on acid secretion before the 8^th week but gave 27 to 32% inhibition thereafter. Gastritis, but not atrophy, appeared between weeks 3 and 7, and persisted up to the 42^nd week . Conclusion. Helicobacter inhibits gastric acid secretion via an H3-receptor pathway and gastritis returns it to normal via a PAF-receptor pathway. This suggests that inflammatory mediators are involved in adaptation to the inhibitory effects of H. pylori on acid secretion.