Role of glucagon in splanchnic hyperemia of chronic portal hypertension.
The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.
D000818:Animals; D005934:Glucagon / Q000276:immunology / Q000502:physiology*; D006940:Hyperemia / Q000209:etiology* / Q000503:physiopathology; D006975:Hypertension, Portal / Q000150:complications*; D007106:Immune Sera / Q000494:pharmacology; D008102:Liver Circulation; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation; D013152:Splanchnic Circulation; D013737:Testis / Q000098:blood supply
D007106:Immune Sera; D005934:Glucagon