WNK kinases regulate sodium chloride and potassium transport by the aldosterone- sensitive distal nephron  A.R. Subramanya, C.-L. Yang, J.A. McCormick, D.H. Ellison  Kidney International  Volume 70, Issue 4, Pages 630-634 (August 2006) DOI: 10.1038/sj.ki.5001634 Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 1 (a) Summary of Xenopus laevis oocyte experiments testing the effects of WNK4 and WNK1 gene products on NCC-mediated Na–Cl co-transport. WNK4-(168–1222), a WNK4 construct that stably suppresses NCC,17 inhibits NCC activity by greater than 50%. L-WNK1 has no direct effect on NCC, but coexpression with WNK4 abrogates the inhibitory effect of WNK4 on NCC, restoring co-transporter activity to near baseline levels. KS-WNK1 has no direct effect on NCC or WNK4; however, KS-WNK1 inhibits L-WNK1-mediated inhibition of WNK4 in a dose-dependent manner (b) Proposed effects of WNK4 and WNK1 gene products on apical sodium and potassium transport pathways in the late renal distal convoluted tubule (DCT2). Under certain physiologic circumstances, aldosterone induces the transcription of KS-WNK1, which helps convert Na+ reabsorption from electroneutral (NCC) to electrogenic (ENaC). This augments potassium secretion by increasing distal flow and luminal Na+ concentration. KS-WNK1 also enhances potassium section by increasing ROMK surface abundance, via its effect on L-WNK1. See text for details. (adapted from Subramanya et al.18) Kidney International 2006 70, 630-634DOI: (10.1038/sj.ki.5001634) Copyright © 2006 International Society of Nephrology Terms and Conditions