Vagally-induced non-adrenergic, non-cholinergic inhibitory motility in the rabbit stomach "in vivo".

In atropine-treated rabbits, electrical stimulation of vagal nerves at low frequency and low basal gastric volumes evoked a biphasic response: rapid onset relaxation followed by rebound contractions. Increase in the frequency of stimulation and/or in basal gastric volume caused a depression of the rebound contraction and a conversion of the biphasic response into a triphasic one: i.e., the post-stimulus excitatory motility was followed by a long-lasting slow relaxation. The rebound contraction, which was mimicked by arterial injections of prostaglandin E2, appears to be a key factor in the conversion of one type of response into the other.