The objective of these studies was to assess the role of gastrointestinal hormones in controlling gastrointestinal motility. In the proximal stomach, cholecystokinin (CCK), gastrin, and secretin inhibit contractions, thereby decreasing intragastric pressure and slowing gastric emptying of liquids. Gastric inhibitory polypeptide (GIP), glucagon, and vasoactive intestinal peptide (VIP) may also slow gastric emptying, since they also inhibit proximal gastric contractions, but this was not tested. In contrast, motilin augments proximal gastric contractions and speeds gastric emptying of liquids. The contractions of the distal stomach are stimulated by gastrin, CCK, and motilin and inhibited by secretin, gastric inhibitory polypeptide, and VIP. The modulation of distal gastric contractions by these hormones may influence gastric trituration and emptying of solids, but this is unknown. Pyloric contractions are enhanced by CCK and secretin, an effect blocked by gastrin. Such enhancement ought to decrease duodenal‐gastric reflux, but again, this is untested. In the small bowel, CCK, gastrin, motilin, VIP, and glucagon stimulate contractions, while secretin inhibits contractions. CCK and motilin speed small bowel transit, but VIP and glucagon slow transit. The cyclical bursts of gastroduodenal contractions that occur during fasting are associated with increased concentrations of motilin in the plasma, whereas the contractions characteristic of the fed state are copied by exogenous administration of gastrin and CCK. Of all these actions, only those of CCK on the proximal stomach, and gastrin on the distal stomach, have been shown to be physiologic so far.