Impaired gallbladder motility plays an important role in the pathogenesis of benign gallbladder disorders. Defective gallbladder muscle contraction is associated with supersaturated bile with cholesterol and with pregnancy due to high circulating levels of progesterone. These abnormalities result in bile stasis that facilitates gallstone growth. A defective gallbladder muscle contraction may also contribute to the pathogenesis of acute and chronic cholecystitis. In addition, an impaired gallbladder contraction may be the source of recurrent biliary colicky pain in patients with acalculus gallbladder disease. The gallbladders of these patients have an abnormal ejection fraction of less than 35% in response to an intravenous infusion of cholecystokinin (CCK). Although histology of the gallbladder wall is grossly normal, the muscle cells are functionally abnormal, with an impaired response to agonists that act on membrane and cytosolic receptors.