1991/06/01 by Arne K. Sandvik, A. K. Sandvik, Helge L. Waldum +1
Biochemistry, Genetics and Molecular Biology · Medicine · Neuroscience · #Helicobacter pylori-related gastroenterology studies #Ion Transport and Channel Regulation #Neuropeptides and Animal Physiology
paper · doi:10.1152/ajpgi.1991.260.6.g925
openalex publication_date 1991/06/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29
To study the interdependence between gastric histamine release and acid secretion, we examined the effects of gastrin-(1-17) [G-(1-17)] or cholecystokinin-(1-33) [CCK-(1-33)] alone or combined with the gastrin (CCK-B) antagonist L365,260 or the CCK-A antagonist L364,718 in the isolated vascularly perfused rat stomach. G-(1-17) and CCK-(1-33) gave concentration-dependent increases in acid secretion and histamine release. Gastrin or CCK-A antagonist alone did not stimulate histamine release or acid secretion. Maximally G-(1-17) or CCK-(1-33) stimulated histamine release and acid secretion was unchanged by the CCK-A antagonist, while the gastrin antagonist induced a parallel and concentration-dependent decrease in stimulated histamine and acid secretion. We conclude that G-(1-17) and CCK-(1-33) stimulate histamine and acid secretion by a CCK-B (gastrin) receptor. The present results indicate that gastrin, at least in this species, stimulates acid secretion by releasing histamine.