Intravenous administration of cholecystokinin octapeptide (CCK-8) to urethane-anesthetized rats produced both inhibitory and excitatory effects on intestinal motility. The inhibitory effect, evident as a transient relaxation or inhibition of distension-induced reflex contractions, was abolished by adrenoreceptor blockade, guanethidine pretreatment or removal of the celiac ganglion complex, but was hexamethonium-and atropine-insensitive. The excitatory action of CCK-8 was atropine- and hexamethonium-sensitive, while being unaffected by guanethidine pretreatment. Ligation experiments indicated that the excitatory effect of CCK-8 originates from a stimulant action on structures in the upper duodenum/pyloric sphincter from which a propagated contraction travels to the distal duodenum. We conclude that i.v. CCK-8 inhibits small intestinal motility by directly activating sympathetic neurons in the celiac ganglion and initiates a propagated form of intestinal motility by stimulating neural elements in the upper part of the small intestine.