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Neurohormonal control of biliary secretion and gallbladder function

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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.

Résumé

La formation de bile dépend principalement de l'excrétion des sels biliaires par le foie; celle-ci est contrôlée par la circulation entéro-hépatique qui ramène les sels biliaires au foie, et par la synthèse de nouveaux sels biliaires. Plusieurs hormones gastro-intestinales, la sécrétine, la CCK, la gastrine sulfatée et le glucagon, augmentent le volume de la sécrétion biliaire et l'excrétion biliaire d'électrolytes; mais aucune d'entre elles n'influence la sécrétion de sels biliaires. L'action de la sécrétine est physiologique. La gastrine non sulfatée et la pentagastrine ne sont pas cholérétiques. L'effet cholérétique des dérivés de la CCK dépend de la présence de tyrosine sulfatée en position 7. Les catécholamines augmentent le débit biliaire par un mécanisme qui fait intervenir les récepteurs bêta, mais dont les détails sont encore inconnus. Le rôle du système nerveux parasympathique est mal précisé. Rien ne prouve que la sécrétion hépatique de sels biliaires soit sous contrôle nerveux. Le tonus de la vésicule biliaire et du sphincter d'Oddi contrôle la quantité de bile qui entre dans le duodénum. La CCK est la seule hormone gastro-intestinale dont l'activité cholécystocinétique soit démontrée. Elle provoque la contraction de la vésicule et l'ouverture du sphincter d'Oddi par une action directe sur ces organes. Le système nerveux parasympathique joue probablement un rôle dans la régulation du tonus musculaire de la vésicule.

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Kaminski, D.L., Nahrwold, D.L. Neurohormonal control of biliary secretion and gallbladder function. World J. Surg. 3, 449–456 (1979). https://doi.org/10.1007/BF01556105

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