Caerulein, CCK8, and gastrin, hormones which interact with the cholecystokinin receptor increased the growth of mouse pancreatic acinar cells in vitro. In contrast, bombesin, substance P, and carbachol, factors which interact with separate receptors, and stimulate pancreatic secretion similarly to CCK by mobilising intracellular Ca2+, did not have any effect on the growth of pancreatic acinar cells in vitro. These results suggest both a unique role for cholecystokinin in the physiological regulation of the pancreas and that the mechanisms that mediate the trophic effects of cholecystokinin are different from those that mediate secretion.