Gastrin has been proposed as a trophic factor for the pancreas. Extensive small-bowel resection increased transiently plasma gastrin levels in the rat and produced pancreatic growth. This growth was characterized by an increased pancreatic weight, protein and DNA content, and the occurrence of mitotic figures in acinar cells. in order to determine if gastrin is implicated in pancreatic hyperplasia, we induced endogenous variations of gastrin 3 weeks before small-bowel resection or transection. Hypogastrinernia was produced by antrectomy and hypergastrinemia by vagotomy plus pyloroplasty. Pyloroplasty alone was without any effect. All gastric operations alone enhanced though not significantly the weight of the pancreas and its content in protein and DNA. When performed before intestinal resection, they did not modify the hyperplasic response of the pancreas to the resection. Our findings do not support the views that antral gastrin exerts a trophic action on the rat pancreas and that gastrin is implicated in postresectional hyperplasia of the gland.