Gastrin, Antral G Cells, and Gastric Acid in Secretagogue-Induced and Antihistamine-Inhibited Duodenal Ulcers

Abstract

In fasting control rats there was continuous basal gastric acid secretion, with a low plasma gastrin and antral G-cells full of immunofluorescent gastrin. After subcutaneous infusion of the gastric secretagogues, pentagastrin + carbachol, there was a six-hour period of gastric hypersecretion, but no change in plasma and G-cell gastrin. Pretreatment with the antihistamine derivative, Pfizer UK-9040, decreased both basal and stimulated acid secretion, whereas plasma gastrin levels increased and the antral G-cells were emptied of gastrin. These results suggest that this antihistamine derivative decreases gastric acid secretion by a direct action on the parietal cells and not by reducing gastrin release from the G-cells. The increased release of gastrin from the G-cells may be secondary to decreased gastric acid production, or more probably by a direct stimulation of the antral G-cells.

Key-words:

• Antral G cells
• antihistamine derivative
• duodenal ulcers
• gastric secretion
• gastrin
• secretagogue-induced