Factors influencing the vagally induced rebound contraction and its role in gastric inhibitory motility were studied in the anaesthetised rabbit. Gastric motility was assessed from measurements of gastric volume by means of an intragastric balloon. In the atropine- and guanethidine-treated animals, vagal stimulation caused biphasic motor responses: a rapid relaxation was followed by a rebound contraction. The latter, depending on experimental conditions, was able to restore and maintain gastric volume at the basal level. However, the rebound contraction was greatly influenced by the stimulation parameters and the basal gastric volume. Stimulation periods of less than 30 sec, or stimulation frequencies above 20 Hz, as well as basal gastric volumes above 70 ml could reduce the amplitude of the post-stimulus excitatory motility, and transformed the biphasic response into a triphasic one: a slow, long-lasting relaxation appeared after the rebound contraction. Prostaglandin-synthesis inhibitors of the non-steroidal anti-inflammatory group depressed the rebound contraction, and caused persistence of gastric relaxation, even after the offset of vagal stimulation. PGE2 evoked excitatory motor responses which closely mimicked the vagally induced rebound contraction. PGE2 also interrupted the rapid or slow, long-lasting relaxant responses. PGF2 alpha elicited tonic excitatory responses. These results suggest that PGE2 is involved in the mechanism underlying post-stimulus excitatory motility. They also suggest that the rebound contraction is a key factor in determining the inhibitory motility pattern of the rabbit stomach.