Do Histamine-Storing Cells in the Gastric Mucosa Mediate the Acid-Stimulating Action of Gastrin?
Gastrin is produced in endocrine cells (gastrin or G cells) in the antrum of the stomach and released in response to food intake to act upon the oxyntic gland area. A number of extragastric sites have been proposed as targets for gastrin; however, there is little doubt that the primary target for antral gastrin is the stomach itself. Gastrin evokes the following effects in the acid-producing gastric mucosa: (a) stimulation of acid secretion; (b) stimulation of mucosal growth (cf. Johnson 1985, HÅkanson et al. 1986a,b, 1988; Ryberg et al. 1990); (c) activation of the histamine-containing, peptide hormone-producing endocrine cell population, referred to as enterochromaffin-like (ECL) cells (cf. HÅkanson et al. 1984); and (d) mobilization of a blood calcium-lowering hormone, referred to as gastrocalcin (HÅkanson et al. 1987, 1989, 1990; Persson et al. 1989). It is probable that all four effects are physiologically important, since they can be demonstrated at serum gastrin concentrations corresponding to those that occur postprandially. Gastrin-stimulated growth of the gastric mucosa has been demonstrated both experimentally and clinically (cf. HÅkanson et al. 1986a). The ECL cells seem to respond better to the trophic action of gastrin than do the other mucosal cell types (Ryberg et al. 1990). Gastrin-stimulated activation of the ECL cells is reflected in mobilization and secretion of histamine and activation of the histamine-forming enzyme histidine decarboxylase (cf. HÅkanson et al. 1984).
KeywordsCholine Acetylcholine Cimetidine Omeprazole Atropine
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