Studies in dogs suggest that bombesin-stimulated pancreatic exocrine function is mediated via endogenous cholecystokinin. We studied (a) the short-term effects of bombesin on pancreatic juice volume and protein output in unconscious rats and (b) whether a potent cholecystokinin-receptor antagonist, L-364,718, affects the pancreatic exocrine response to bombesin. A 4-h i.v. infusion of low-dose (0.2 nmol/kg.h) or high-dose (1.0 nmol/kg.h) bombesin elicited significant increases in pancreatic juice volume and protein output, which were unaltered by treatment with L-364,718 at a dose capable of fully suppressing cholecystokinin-octapeptide-stimulated pancreatic juice volume and protein output. We conclude that the effects of exogenously administered bombesin on the exocrine pancreas in the rat are not mediated via release of endogenous cholecystokinin.