Effect of gastrin I and gastrin II on canine bile flow.
The role of gastrin in the hormonal control of canine hepatic bile flow was evaluated. Because of the importance of the presence of sulfation of the carboxyl terminal peptide in the function of other cholecystokinetic hormones and peptides in the biliary tract, the choleretic properties of sulfated gastrin II were compared to the choleretic properties of nonsulfated gastrin I. Exogenous administration of gastrin I and II to dogs with chronic bile fistulas demonstrated that gastrin II, but not I, significantly increased hepatic bile flow. Chemical stimulation of the release of endogenous gastrin in dogs with denervated antral pouches did not increase hepatic bile flow, whereas a choleresis resulted when the innervated antrum was stimulated. Serum gastrin values obtained during the infusion of gastrin II at doses that produced a choleresis resulted in serum gastrin values that were greater than those produced by a more physiological stimulus, such as chemical antral stimulation. The results of this study suggest that only the sulfated gastrin II, not gastrin I, is a choleretic agent in dogs and only at pharmacological, not physiological doses.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001646:Bile / Q000378:metabolism / Q000502:physiology*; D002756:Cholagogues and Choleretics; D004285:Dogs; D005755:Gastrins / Q000097:blood / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration
D002756:Cholagogues and Choleretics; D005755:Gastrins; D000109:Acetylcholine