Total or intestine-specific NHE3 deletion is known to result in hyponatremia, acidosis, and a decrease in blood pressure, resulting in massive hyperaldosteronism and strong upregulation of the expression of all ENaC (epithelial sodium channel) subunits, even in the more proximal colonic segments in which ENaC expression is usually very low [25,26]. This evidence concerns the gene SLC9A3 and hyperaldosteronism.