The role of cholecystokinin (CCK) inpostprandial control of colonic motility iscontroversial. To test the hypothesis that CCKstimulates colonic tone, motility, and transit wemeasured these colonic functions in 16 healthy subjects using intraluminalmanometry, barostatic balloon measurements, andradioscintigraphy. This was a randomized-order,double-blind, sequential study design in each subject ofsaline and either atropine (0.01 mg/kg stat and 0.01mg/kg/hr by infusion) or CCK-octapeptide (OP, 30 ng/kgstat and 60 ng/kg/hr by infusion). Atropine was used ascontrol to demonstrate responsiveness of selected parameters of colonic motility. Atropinesignificantly reduced whole colon (change from fasting= 52 ± 11%) and left colon (change from fasting61 ± 8%) phasic pressure activity and transversecolon tone (change from fasting 159 ± 40%); CCK-OP had nosignificant effects on phasic contractility, tone ortransit. Thus, a CCK-OP infusion that maximallystimulates pancreatic exocrine secretion and gallbladdercontraction has no effect on motor function or transit inprepared colon of healthy subjects.