Role of acetylcholine and gastrin-releasing peptide (GRP) in gastrin secretion.

Using an isolated rat stomach infusion model, we investigated the role of gastrin-releasing peptide (GRP) and acetylcholine in the secretion of gastrin (which plays a major role in gastric acid secretion), and the relationship between gastrin secretion and stomach pH. Bombesin, which has a structure analogous to that of GRP, was used in the experiment. We also investigated whether acetylcholine has muscarine-like or nicotine-like action. Our findings pointed to the presence of an alternative, GRP-mediated, route for stimulating gastric secretion from G cells, other than the acetylcholine-mediated route. We injected bombesin to confirm the presence of such a GRP-mediated route; significantly increased gastrin secretion was observed, even under acidic conditions, in the gastric lumen, which has been considered to show almost no gastric secretion. This secretion was not inhibited by atropine. The results suggested that there are two routes for inducing gastrin secretion from G cells: an acetylcholine-mediated route and a GRP-mediated route (intramural peptide neurons). As GRP induced gastrin secretion, regardless of stomach pH, GRP was considered to be more closely related to gastrin secretion. The results also suggested that a muscarine-like action, particularly in the M3 receptor-mediated route, plays a significant role in acetylcholine-mediated gastrin secretion and that nicotine-like action is not involved in gastrin secretion.