The content of kallikreinogen in the pancreas isolated from rats with acute experimental pancreatitis rose to over ten times the level in the control group. In the isolated and perfused pancreata prepared from the pancreatitis group; the "resting" leak of kallikreinogen into the portal perfusate was 8 times that in the control group, and it was further increased by stimulation with CCK (5 mU/ml). The "resting" amylase level in the portal perfusate was 5 times that in the control group, but stimulation with CCK caused no further increase. The results suggest that kallikrein formation may be an important step in the development of acute pancreatitis.