Gastrin, antral g cells, and gastric acid in secretagogue-induced and antihistamine-inhibited duodenal ulcers.
Scand J Gastroenterol, 1977;12(1):27-32.
Joffe SN, Polak JM, Pallone F, Bloom SR, Gaskin RJ, Barros D'sa AA, Baron JH
PMID: 13481
Impact factor: 3.027
Abstract
In fasting control rats there was continuous basal gastric acid secretion, with a low plasma gastrin and antral G-cells full or immunofluroescent 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.
MeSH terms
Animals; Carbachol; Duodenal Ulcer; Fluorescent Antibody Technique; Gastric Juice; Gastrins; Histamine H2 Antagonists; Male; Microscopy, Electron; Pentagastrin; Pyloric Antrum; Pyrrolidines; Rats; Rats, Inbred Strains; Secretory Rate; Thiophenes; Time Factors
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