To investigate the pathogenesis of diarrhea in inflammatory bowel disease, electrolyte transport was examined in vitro in stripped colonic mucosa taken from the sigmoid or descending colon in colectomy specimens. Compared with previously reported values from normal colon, the electrical potential difference, short circuit current, and mucosal resistance were significantly lower in diseased mucosa. This reduction was associated with a significantly lower net sodium absorption in diseased mucosa, owing to a reduced mucosa to serosa unidirectional flux. Net chloride flux was similar to normal, but unidirectional fluxes were reduced. In mucosa from patients treated with corticosteroids, fluxes were similar to normal, while in untreated patients they were markedly impaired. It is concluded that there is a defect in active sodium absorption in inflammatory bowel disease that may contribute to the diarrhea. A secretory process, inhibited by sulphasalazine, cannot be excluded however.