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1 Department of Internal Medicine, Yale University, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: henry.binder{at}yale.edu.
Zn, an essential micronutrient and second most abundant trace element in cell and tissues, reduces stool output when administered to children with acute diarrhea. The mechanism by which Zn improves diarrhea is not known but could result from stimulating Na absorption and/or inhibiting anion secretion. The aim of this study was to investigate the direct effect of Zn on intestinal epithelial ion absorption and secretion. Rat ileum was partially stripped of serosal and muscle layers and the mucosa was mounted in lucite chambers. Potential difference and short-circuit-current was measured by conventional current-voltage clamp method. 86Rb efflux and uptake were assessed for serosal K channel and Na-K-2Cl cotransport activity, respectively. Efflux experiments were performed in isolated cells preloaded with 86Rb in the presence of ouabain and bumetanide while, uptake experiments were performed in low Cl isotonic buffer containing Ba and ouabain. Neither mucosal nor serosal Zn affected glucose-stimulated Na absorption. In contrast, forskolin-induced Cl secretion was markedly reduced by serosal but not mucosal addition of Zn. Zn also substantially reversed the increase in Cl secretion induced by 8-Br-cAMP with an IC50 of 0.43 mM. In contrast, serosal Zn did not alter Cl secretion stimulated by carbachol, a Ca-dependent agonist. Zn inhibited 8-Br-cAMP-stimulated 86Rb efflux but not carbachol-stimulated 86Rb efflux. Zn had no effect on bumetanide-sensitive 86Rb uptake, Na-K-ATPase or CFTR. We conclude from these studies that Zn inhibits cAMP-induced Cl secretion by blocking basolateral membrane K channels.
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