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Loss of Ca2+‐mediated ion transport during colitis correlates with reduced ion transport responses to a Ca2+‐activated K+ channel opener

Background and purpose:  Epithelial surface hydration is critical for proper gut function. However, colonic tissues from individuals with inflammatory bowel disease or animals with colitis are hyporesponsive to Cl‐ secretagogues. The Cl‐ secretory responses to the muscarinic receptor agonist bethanechol are virtually absent in colons of mice with dextran sodium sulphate (DSS)‐induced colitis. Our aim was to define the mechanism underlying this cholinergic hyporesponsiveness.