Double Knockout of the Na+-Driven Cl-/HCO3- Exchanger and Na+/Cl- Cotransporter Induces Hypokalemia and Volume Depletion.

ABSTRACT: We recently described a novel thiazide-sensitive electroneutral NaCl transport mechanism resulting from the parallel operation of the Cl^-/HCO₃^- exchanger pendrin and the Na⁺-driven Cl^-/2HCO₃^- exchanger (NDCBE) in β-intercalated cells of the collecting duct. Although a role for pendrin in maintaining Na⁺ balance, intravascular volume, and BP is well supported, there is no in vivo evidence for the role of NDCBE in maintaining Na⁺ balance. Here, we show that deletion of NDCBE in mice caused only subtle perturbations of Na⁺ homeostasis and provide evidence that the Na⁺/Cl^- cotransporter (NCC) compensated for the inactivation of NDCBE. To unmask the role of NDCBE,

SUBMITTER: Sinning A 

PROVIDER: S-EPMC5198265 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature