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The gastrocolic reflex or gastrocolic response is one of a number of physiological reflexes controlling the motility, or peristalsis, of the gastrointestinal tract. It involves an increase in motility of the colon in response to stretch in the stomach and byproducts of digestion in the small intestine. Thus, this reflex is responsible for the urge to defecate following a meal. The small intestine also shows a similar motility response.

The reflex was demonstrated by myoelectric recordings in the colons of animals and humans, which showed an increase in electrical activity within as little as 15 minutes after eating. The recordings also demonstrated that the gastrocolic reflex is uneven in its distribution throughout the colon. The sigmoid colon is more greatly affected than the right side of the colon in terms of a phasic response; however, the tonic response across the colon is uncertain. When pressure within the rectum becomes increased, the gastrocolic reflex acts as a stimulus for defecation. A number of neuropeptides have been proposed as mediators of the gastrocolic reflex. These include serotonin, neurotensin, cholecystokinin (CCK), and gastrin.

Clinically, the gastrocolic reflex has been implicated in pathogenesis of irritable bowel syndrome: the very act of eating or drinking can provoke an overreaction of the gastrocolic response in some patients with irritable bowel syndrome due to their heightened visceral sensitivity, and this can lead to abdominal pain, diarrhoea, or constipation.^[1] Also, the serotonin (5HT₃) antagonist ondansetron decreases the tonic response to stretch.

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