Apelin is the endogenous ligand of the G protein‐coupled receptor APJ. The apelinergic system and APJ receptors are widely expressed in gastrointestinal (GI) tissues including stomach, small intestine and colon, suggesting that peripheral apelin may have a regulatory role in GI motor functions. It has been shown that peripheral exogenous administration of apelin increases the release of cholecystokinin (CCK), a well‐defined GI hormone that disturbs gastric emptying (GE), colon transit (CT) and small intestinal fasting motor pattern through CCK‐1 receptors expressed on vagal afferent nerves. The present study was designed to investigate (1) the effects of peripherally administered apelin on GI motor functions and (2) the contribution of CCK in apelin‐induced alterations. For measuring solid GE, rats were given a 1.6 g of preweighed pellet following an overnight fasting. Rats were euthanized 90 min after the completion of feeding and the gastric contents were recovered, dried, and weighed. To measure CT, a silicone catheter was inserted into the proximal colon and fixed with silk sutures; whereas, a strain gage transducer was implanted on the serosal surface of duodenum for recording of intestinal fasting motor pattern. The catheter and the wires of transducer were tunneled subcutaneously and secured to the neck skin. The measurements and recordings were performed after a 7‐day recovery period. For CT measurement, 1.5 ml of phenol red solution was injected through the catheter and rats were euthanized 90 min after injection. The entire colon was removed and divided into 6 equal segments. CT was calculated as the geometric center of distribution of phenol red. In control rats, GE was found 60.1 ± 3.5%; whereas, apelin‐13 administration (100 μg, ip) significantly (p<0.05) delayed the gastric emptying 31.3 ± 2.8%. The apelin‐induced delayed GE was significantly (53.3 ± 5.8%, p<0.05) accelerated by pretreatment of CCK‐1 receptor antagonist lorglumide (2.5 mg, ip) and restored to the control level. Compared with control rats (4.1 ± 0.1), apelin‐13 significantly inhibited CT (3.2 ± 0.1%, p<0.01). However, pretreatment of lorglumide significantly attenuated (4.1 ± 0.1, p<0.05) the inhibitory effect of peripheral apelin administration. The fasting‐induced duodenal phase‐III‐like contractions were remarkably disturbed following apelin‐13 administration. However, pretreatment of lorglumide abolished the apelin‐induced alterations in intestinal fasting motor pattern. These findings suggest that peripheral apelin inhibits GI motor functions and the inhibitory effects of apelin appear to be CCK‐dependent. Peripheral apelin may have a regulatory role in postprandial changes in alimentary motor functions.Support or Funding InformationThis work is funded by The Scientific and Technological Research Council of Turkey (TUBITAK). (Research Programme 1001; project number 214S349).