Neurohormonal control of biliary secretion and gallbladder function

Abstract

The primary determinant of bile formation is the hepatic excretory rate of bile salts, which is controlled by the rate of return of bile salts to the liver by the enterohepatic circulation and by the synthesis of new bile salts. The gastrointestinal hormones secretin, cholecystokinin (CCK), sulfated gastrin, and glucagon increase bile volume and inorganic ion excretion into bile, but none of them influence bile salt secretion. The action of secretin is clearly physiologic. Nonsulfated gastrin and pentagastrin are not choleretics. The choleretic property of CCK derivatives is dependent upon the presence of sulfated tyrosine at position 7. Catecholamines increase bile flow by a mechanism that involves beta receptors, but the precise mechanism is unknown. The role of the parasympathetic nervous system is not clear. There is no evidence that hepatic secretion of bile salts is under neural control. The tone of the gallbladder and sphincter of Oddi regulates the amount of bile that actually enters the duodenum. CCK is the only known physiologic cholecystokinetic gastrointestinal hormone. It contracts the gallbladder and relaxes the sphincter of Oddi by direct action on the muscle of these structures. The parasympathetic nervous system probably participates in regulation of gallbladder muscle tone.Bile salts, the primary constituents of bile, participate in digestion of fats and the absorption of lipids. Bile also serves as the vehicle for hepatic excretion of bilirubin, phospholipids, cholesterol, and some lipid soluble drugs and metabolites that cannot be eliminated by the kidney.Bile formation begins in bile canaliculi, 0.6-1.2/zm channels that are formed by portions of the

The relationship between glucagon and prostaglandin f in stimulating canine hepatic bile flow

“…These results are compatible with the hypothesis that the choleresis produced by glucagon is due in part to the intermediary activity of PGF2, (22).…”

“…Glucagon increased bile flow and bile chloride secretion, and indomethacin inhibited this response. These results are compatible with the hypothesis that the choleresis produced by glucagon is due in part to the intermediary activity of PGF2, (22).…”

“…PGF is present in bile in concentrations four times greater than that in plasma (13). Being a strong choleretic with the ability to increase chloride concentration and output in bile (11,12) suggested it may play a role in glucagon choleresis (22). Current theoretical information concerning the function of the prostaglandins suggests that they may act as intracellular or cell membrane mediators of hormonal stimuli (31).…”

“…We have postulated that PGFz, is a mediator of glucagon choleresis (22). In the present research, we will evaluate the effect of indomethacin, a prostaglandin synthetase inhibitor (23), on glucagon-stimulated bile flow.…”

Adrenergic influence on bile secretion—an experimental study in the cat

“…1985), although contradictory findings have also been reported (Harty et RI. 1973, Kaminski & Narwold 1979. T h e findings in the present study of a reduction of bile flow but not of the bile salt secretion rate, in response to both z-adrenergic and ,8-adrenergic stimulation, inbicates that the bile acid-independent fraction of the canalicular secretion was affected, or that there was an enhanced absorption of water by the biliary epithelium in the bile ducts, as seen in the gallbladder (Bjorck rt a/.…”