Abstract
In the atropine-treated rabbit, vagal stimulation, arterial infusion of ATP or vasoactive intestinal peptide (VIP) caused agastric relaxation. At the end of either vagal stimulation or ATP infusion, but not after VIP, the gastric inhibitory responses were abruptly interrupted by ''rebound contractions''. Administration of fenoprofen depressed or abolished the rebound contraction, thus transforming the brisk relaxant response, elicited by vagal stimulation or ATP, into long-lasting relaxation. Indomethacin depressed the rebound contractions only at high doses and this effect was not always reproducible.