Effect of bombesin and related peptides on the release and action of intestinal hormones on pancreatic secretion.

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Abstract
Pancreatic volume from and bicarbonate and protein secretion from pancreatic fistulas were measured in response to i.v. infusion of graded doses of bombesin [from Bombina frog] and related peptides containing the COOH-terminal fragment of the bombesin molecule in conscious dogs with intact antrum and in anesthetized animals with antrectomy, or antrectomy and enterectomy. Bombesin and related peptides given to conscious dogs produced a potent and dose-dependent increase in pancreatic protein output reaching a maximum equal to that induced by the octapeptide of cholecystokinin (OP-CCK) and a small rise in bicarbonate output attaining a peak amounting to about 10% of that evoked by secretin. The serum gastrin level rose progressively during the infusion of bombesin to reach a peak with the highest dose of the peptide. Bombesin infused i.v. in anesthetized animals with resected antrum evoked a marked increase in pancreatic protein secretion without significant change in the serum gastrin level. Following the removal of the antrum and small intestine, bombesin failed to show any stimulation of the pancreatic secretion or any change in serum gastrin level. The strong stimulatory action of bombesin and related peptides on pancreatic secretion cannot be entirely ascribed to the release of gastrin but might be attributed at least in part to the release of intestinal hormones, particularly CCK. Atropine and the growth hormone-release inhibiting hormone (GH-RIH), which inhibit the release of CCK induced by duodenal perfusion of an amino acid mixture, also caused the inhibition of pancreatic protein secretion by bombesian but failed to affect the pancreatic response to OP-CCK. Bombesin releases, in addition to gastrin, CCK from the gut by a mechanism largely dependent upon cholinergic innervation.