Control of gallbladder contractions by cholecystokinin through cholecystokinin-A receptors in the vagal pathway and gallbladder in the dog.

The mechanism of CCK action on gallbladder contractions in the physiological condition is unclear. Gallbladder contractions were monitored by means of chronically implanted force transducers in conscious dogs. Postprandial gallbladder contractions were partially inhibited by atropine and hexamethonium, and completely inhibited by devazepide. In vitro contractile response of canine gallbladder muscle strips to CCK-8 was also studied. CCK-8-induced muscle strip contraction was atropine and tetrodotoxin resistant, but was completely eliminated by devazepide. The existence of CCK receptors in the vagal nerve and gallbladder was examined by means of autoradiography. Forty-eight hours after ligation of the abdominal vagus, CCK-8 binding sites were found to accumulate in the subdiaphragmatic vagal nerve immediately proximal to the ligature, and similar binding sites were also found in the gallbladder smooth muscle layer. These binding sites were displaced by the addition of 10(-7) mol/1 unlabeled CCK-8 and devazepide, but L-365,260 had no effect. In conclusion, it is considerable that postprandial CCK-induced gallbladder contractions are controlled through CCK-A receptors both on the vagal nerve in stimulating endogenous release of acetylcholine and on the gallbladder directly to stimulate muscle contraction in the dog.