The Relationship Between Glucagon and Prostaglandin F in Stimulating Canine Hepatic Bile Flow

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Abstract
Both glucagon and prostaglandin F2α have been shown to stimulate a chloride–rich choleresis in dogs. This study was performed to ascertain the interrelationship between glucagon and prostaglandin F2α in stimulating bile flow. The experiments were performed using dogs with chronic biliary and gastric fistulas. Initially, the effects of prostaglandin F2α on serum glucagon levels were evaluated. Glucagon administration increased bile volume andchloride secretion as did prostaglandin F2α. Serum glucagon levels during prostaglandin F2α administration were increased significantly over baseline values. During prostaglandin F2α administration, the increase in serum glucagon concentration correlated well with the increase in hepatic bile flow. Administration of somatostatin, a hormone known to inhibit glucagon release, prevented the choleresis produced by prostaglandin F2α while simultaneously eliminating the hyperglucagonemia. Subsequently, the effects of glucagon on bile prostaglandin F secretion and the effect of prostaglandin synthetase inhibition on glucagon choleresis were evaluated. Bile prostaglandin F secretion increased from control values of 101 ± 27 pg per min (mean ± S.D.) during bile salt infusion alone to 1,498 ± 1,086 pg per min during the administration of 1 μg kg-1 hr-1 glucagon. The prostaglandin synthetase inhibitor, indomethacin, significantly decreased the choleresis, the increased bile chloride secretion and the increased bile prostaglandin F secretion produced by glucagon. The results of this study indicate that prostaglandin F2α-stimulated bile flow is primarily the result of glucagon release and suggest that prostaglandin F2α may be involved in glucagon secretion. The inhibition of glucagon choleresis by indomethacin is compatible with the hypothesis that prostaglandin F2α partially mediates the response of the hormone associated with increased chloride secretion. Prostaglandin F2α may be involved in glucagon choleresis both during release of the hormone and at the site of its action.