Central corticotropin-releasing factor (CRF) plays an important role in mediating restraint stress-induced delayed gastric emptying. However, it is unclear how restraint stress modulates gastric motility to delay gastric emptying. As a solid gastric emptying is regulated via antro-pyloric coordination, we hypothesized that restraint stress impairs antro-pyloric coordination resulting in delayed solid gastric emptying in conscious rats. Two strain gauge transducers were sutured on the serosal surface of the antrum and pylorus. Postprandial gastric motility was monitored before, during and after the restraint stress. Antro-pyloric coordination was defined as a propagated single contraction from the antrum to pylorus within 10 sec and was followed by quiescence at least 20 sec. Restraint stress enhanced the postprandial gastric motility in the antrum and pylorus to 140±9% and 134±9% of basal, respectively (n=6). The number of episodes of antro-pyloric coordination was 2.4±0.4/10 min before the restraint stress, which was significantly reduced to 0.6±0.3/10 min by restraint stress. Intracisternal (IC) injection of CRF type2 receptor antagonist, astressin₂-B (60 µg), or guanethidine partially restored restraint stress-induced impairment of antro-pyloric coordination (1.6±0.3/10 min, n=6). The restraint stress-induced augmentation of antral and pyloric contractions were increased by astressin₂-B and guanethidine, but abolished by atropine, hexamethonium and vagotomy. Restraint stress enhanced postprandial gastric motility via a vagal cholinergic pathway. Restraint stress-induced delay of solid gastric emptying is due to the impairment of antro-pyloric coordination. Restraint stress-induced impairment of antro-pyloric coordination might be mediated via a central CRF pathway.