The exact mechanism by which cisapride exerts its prokinetic effects is not known. It has been shown that it acts as both an agonist and antagonist at serotonin receptors throughout the GI tract. D The resultant clinical effects seen with cisapride therapy include decreased exposure of the esophagus to gastric acid, increased lower esophageal sphincter pressure and esophageal motility, accelerated gastric emptying of both liquids and solids, and decreased colonic transit time. Consequently, these actions contribute to the relief of symptoms and the healing of lesions associated with reflux disease. Peak plasma levels occur 1-2 hours after administration.
Metabolism is extensive with no active metabolites.
The elimination half-life of cisapride is about 10 hours in healthy volunteers and may be prolonged in patients with hepatic impairment or in the elderly. Cisapride pharmacokinetics are not altered in patients with renal impairment or in patients receiving hemodialysis. Cisapride is classified as pregnancy category C. Adequate studies in pregnant women have not been conducted, so cisapride should be used during pregnancy only when clearly needed. Cisapride is excreted into breast milk at a concentration of about one twentieth that found in maternal plasma. Caution is advised in prescribing cisapride to breast-feeding women.