Pendrin-null mice develop severe hypokalemia following dietary Na<sup>+</sup> and K<sup>+</sup> restriction: role of ENaC
Truyen D. Pham, Anthony Elengickal, Jill W. Verlander, Lama Al‐Qusairi, Chao Chen, Delaney C. Abood, Spencer King, Johannes Loffing, Paul A. Welling, Susan M. Wall
Abstract
Pendrin is an apical Cl − /[Formula: see text] exchanger that provides renal K + -sparing NaCl absorption. The pendrin-null kidney has an inability to fully conserve K + and limits renal K + loss by downregulating the epithelial Na + channel (ENaC). However, with Na + restriction, the need to reduce ENaC for K + balance conflicts with the need to stimulate ENaC for intravascular volume. Therefore, NaCl restriction stimulates ENaC less in pendrin-null mice than in wild-type mice, which mitigates their kaliuresis and hypokalemia but exacerbates volume contraction.
Topics & Concepts
PendrinKaliuresisEpithelial sodium channelInternal medicineEndocrinologyHypokalemiaChemistryKidneyNatriuresisBiologyMedicineSodiumBiochemistryTransporterOrganic chemistryGeneIon Transport and Channel RegulationRenal function and acid-base balanceElectrolyte and hormonal disorders