[Neurohormonal regulation of gallbladder motility]

The motility of the gallbladder (GB) consists of collection, storage and delivery of bile. GB motor functions are controlled by its extrinsic and intrinsic innervation, and humoral factor. In the fasting stage, GB motility is associated with phase 3 of the interdigestive migrating myoelectric complex and increased plasma motilin concentrations. In the fed state cholecystokinin (CCK) is the primary mediator of GB contraction. Extrinsic neural control of GB motility appears to play a role in the mediation of cephalic phase of GB emptying. Vagal stimulation induces GB concentration, and sympathetic stimulation induces GB relaxation via cholinergic, adrenergic, and noncholinergic, nonadrenergic neurotransmitters. Intrinsic neural control of GB motility is mediated by such neuropeptides as pancreatic polypeptide, somatostatin, bombesin, neuropeptide Y, calcitonin gene-related peptide, vasoactive intestinal polypeptide, CCk, tachykinins and nitric oxide.