Abstract
Gallbladder pressure was measured by a pressure transducer inserted into the gallbladder lumen. Infusion of CCK8 (2.5-80 ng/kg/min) increased gallbladder pressure in a dose-dependent fashion. Atropine, hexamethonium and truncal vagotomy antagonized gallbladder responses to low doses of CCK8 (2.5-5 ng/kg/min) but had no effect on doses above 10 ng/kg/min. Atropine or hexamethonium had no further inhibitory effect on guinea pigs which had undergone truncal vagotomy. Fasted guinea pigs achieved a postprandial peak plasma CCK level of 8 pM, which was most closely approximated by the 5 ng/kg/min intravenous CCK8 infusion. CCK8 (5 ng/kg/min)-induced contraction was significantly reduced by chronic treatment with sensory neurotoxin, capsaicin. Doses of CCK8 which produce physiologic plasma CCK levels are suggested to act via stimulation of sensory neurons and presynaptic cholinergic neurons in a vagal nerve and finally stimulate the release of acetylcholine from nerve terminals of postsynaptic cholinergic neurons, whereas infused doses of CCK8 which produce supraphysiologic CCK levels may act directly on gallbladder smooth muscle.
