| Abstract: | The effects of gastrin precursors have been discussed during recent years. However, the mechanism for their action, whether through a novel receptor on the parietal cell or a cholecystokinin‐2 (CCK‐2) receptor on the enterochromaffin like (ECL) cells, is still not settled. This study examines the effect of glycine‐extended gastrin‐17 (Gly‐G‐17), the main non‐amidated gastrin precursor, on gastric acid secretion and histamine release in the totally isolated vascularly perfused rat stomach. Glycine‐extended gastrin‐17 at the concentrations from 0.52 to 520 nmol L–1 was administered to the totally isolated vascularly perfused rat stomach. Glycine‐extended gastrin‐17 at 52 or 520 nmol L–1, and gastrin‐17 at 0.52 nmol L–1 were co‐administered to examine whether glycine‐extended gastrin augmented maximal gastrin stimulated acid secretion and histamine release. Both Gly‐G‐17 at 52 nmol L–1 and gastrin‐17 (G‐17) at 0.52 nmol L–1 were administered together with the histamine‐2 receptor antagonist ranitidine at 10 μmol L–1. Gastric acid and venous histamine output were measured. Glycine‐extended gastrin‐17 at lower concentrations from 0.52 to 5.2 nmol L–1 did not stimulate gastric acid output or histamine release, whereas higher concentrations from 52 to 520 nmol L–1 elicited a concentration‐dependent increase in acid secretion and histamine release. The outputs of acid and histamine at 520 nmol L–1 Gly‐G‐17 were at the same level as those found for G‐17 at its maximally effective concentration of 0.52 nmol L–1. Glycine‐extended gastrin‐17 at maximally effective concentration of 520 nmol L–1 did not augment maximal gastrin stimulated acid secretion or histamine release. Ranitidine inhibited G‐17 and Gly‐G‐17 stimulated acid secretion to a similar degree. This study confirms that the stimulatory effect of Gly‐G‐17 on gastric acid secretion is via a CCK‐2 receptor on the ECL cell. |
