Serotonin-induced alteration of colonic electrolyte transport in the rat

Abstract

Serotonin, a calcium-dependent intestinal secretagogue, inhibits sodium chloride absorption in the rabbit ileum, but unlike cyclic adenosine monophosphate-dependent secretagogues, does not stimulate chloride secretion. Because bethanechol, a muscarinic cholinergic agonist that acts as a calcium-dependent, noncyclic adenosine monophosphate-mediated secretagogue, both inhibits sodium chloride absorption and stimulates active chloride secretion in the rat colon, experiments were performed with serotonin to determine the effect of serotonin on colonic ion transport. In luminal perfusion studies, intravenous infusion of serotonin significantly decreased net water and net sodium transport. In in vitro studies of sodium and chloride transport performed under short circuit conditions, serotonin decreased both net sodium and net chloride absorption and increased short circuit current (1.7 ± 0.4, 4.0 ± 0.6, and 2.3 ± 0.3 μEq/h · cm2, respectively). The decrease in net chloride transport was significantly greater than that in net sodium absorption and the difference between these changes was equivalent to the change in short circuit current. Removal of serosal calcium inhibited all of the effects of serotonin on electrolyte transport. Tetrodotoxin, an inhibitor of neurotransmission, had no effect on serotonin-induced changes in electrolyte transport. These results demonstrate that serotonin both inhibits neutral sodium chloride absorption and stimulates active chloride secretion by a calcium-dependent process in the rat colon.