N-Methyl scopolamine (NMS) 25 mg kg-1 was given to rats for 14 days as a single daily intraperitoneal injection or by constant infusion through osmotic minipumps placed in the abdominal cavity. The anticholinergic drug reduced significantly body and pancreatic weights, and total pancreatic DNA contents, an indication of tissue growth inhibition. Total enzyme and protein contents were however significantly increased with the drug infusion more efficiently than by the daily injection. It is suggested that pancreatic hypertrophy observed after NMS treatment can be ascribed partially to inhibition of enzyme release elicited by blocking the enteropancreatic reflex causing over a long period enzyme accumulation in the gland. In conclusion, chronic anticholinergic treatment resulted in pancreatic aplasia and hypertrophy and could serve as a good model to study muscarinic receptor modulation in the pancreas.