Effect of bombesin antagonist D-Phe 6-BN(6-13)OMe on vagally induced gastrin release from perfused rat stomach

Abstract

The aim of the present study was to evaluate the effect of the bombesin antagonist D-Phe 6-BN(6-13)OMe (BN-antagonist) on vagally stimulated gastrin release from the isolated rat stomach, which was perfused via the celiac artery with Krebs-Ringer buffer. Vagal stimulation was performed for 10 minutes with 1 ms, 10 V and 10 or 2 Hz, respectively. Gastrin secretion increased significantly during stimulation with 10 and 2 Hz. BN-antagonist was added to the perfusate at the concentration of 10 −6 M, which induced a significant reduction of vagally stimulated gastrin release at 10 Hz (619 ± 65 vs. 252 ± 62 pg/10 min, p<0.05), but not at 2 Hz (564 ± 117 vs. 493 ± 113 pg/10 min, p>0.05). In contrast, atropine (10 −7 M) reduced significantly the gastrin response at 2 Hz (270 ± 78 pg/10min, p<0.01), but not at 10 Hz (446 ± 87 pg/10 min, p>0.05). The combination of BN-antagonist and atropine elicited an inhibition of vagally stimulated gastrin release similar to each substance when given alone. Basal gastrin release was not changed by the BN-antagonist. The present data suggest, that in the rat stomach endogenously released bombesin-related peptides contribute to the noncholinergic stimulation of gastrin release at higher stimulation frequencies (10 Hz), however, bombesin-related peptides are not involved, when lower stimulation frequencies (2 Hz) are employed. At both stimulation frequencies additional mechanisms are activated which are noncholinergic and not related to bombesin peptides.