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Am J Physiol Gastrointest Liver Physiol 278: G570-G577, 2000;
0193-1857/00 $5.00
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Vol. 278, Issue 4, G570-G577, April 2000

Mechanism of glucocorticoid-mediated reversal of inhibition of Clminus /HCOminus 3 exchange during chronic ileitis

Steve Coon and Uma Sundaram

Division of Digestive Diseases, Departments of Medicine and Physiology, Ohio State University School of Medicine, Columbus, Ohio 43210

In the normal ileum, coupled NaCl absorption occurs via the dual operation of Na+/H+ and Cl-/HCO-3 exchange on the brush-border membrane (BBM) of villus cells. In a rabbit model of chronic small intestinal inflammation we determined the cellular mechanism of inhibition of NaCl absorption and the effect of steroids on this inhibition. Cl-/HCO-3 but not Na+/H+ exchange was reduced in the BBM of villus cells during chronic ileitis. Cl-/HCO-3 exchange was inhibited secondary to a decrease in the affinity for Cl- rather than an alteration in the maximal rate of uptake of Cl- (Vmax). Methylprednisolone (MP) stimulated Cl-/HCO-3 exchange in the normal ileum by increasing the Vmax of Cl- uptake rather than altering affinity for Cl-. MP reversed the inhibition of Cl-/HCO-3 exchange in rabbits with chronic ileitis. However, MP alleviated the Cl-/HCO-3 exchange inhibition by restoring the affinity for Cl- rather than altering the Vmax of Cl- uptake. These data suggest that glucocorticoids mediate the alleviation of Cl-/HCO-3 exchange inhibition in chronically inflamed ileum by reversing the same mechanism that was responsible for inhibition of this transporter rather than exerting a direct effect on the transporter itself, as was the case in normal ileum.

glucocorticoids; inflammatory bowel disease; chloride/bicarbonate exchange; sodium/hydrogen exchange; coupled sodium chloride absorption; immune regulation of electrolyte transport


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