Previous studies have suggested that enterohepatic circulation of bile acids is essential for regular cycling of duodenal migrating motor complexes (MMCs). The present study was an attempt to clarify the role of bile acids in the enterohepatic circulation system in initiating duodenal MMCs. Seven dogs underwent total external biliary diversion that resulted in the loss of MMCs originating from the duodenum. Sodium ursodeoxycholate (6 mg/kg/hr) was then given either through the portal vein or a peripheral vein, and motility of the gastrointestinal tract was serially recorded. When sodium ursodeoxycholate was given either through the portal vein or a peripheral vein during external biliary diversion, duodenal MMCs restarted. The cyclic change in plasma motilin levels during an MMC cycle as induced by sodium ursodeoxycholate was almost the same as in a normal MMC cycle. Total bile acid concentration in the portal vein changed cyclically with MMC cycles when bile flow was intact but did not change cyclically with MMC cycles restarted by intravenous bile salt infusion. Bile acid stimulation of putative receptors existing between the portal vein and intrahepatic bile ducts may be involved in initiating normal duodenal MMC cycles.