Neurohormonal control of biliary secretion and gallbladder function

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.