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The disruption of KCNJ10 stimulates the expression of Na‐activated K channel in the basolateral membrane of the thick ascending limb
Author(s) -
Zhang Chengbiao,
Wang Lijun,
Su Xiaotong,
Lin Daohong,
Wang Wenhui
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.968.3
Subject(s) - immunostaining , distal convoluted tubule , chemistry , epithelial polarity , patch clamp , endocrinology , medicine , biophysics , biology , electrophysiology , membrane , anatomy , kidney , neuroscience , nephron , biochemistry , immunohistochemistry
Previous study has demonstrated that the disruption of Kcnj10 decreased the expression of NCC in the distal convoluted tubule (DCT). The aim of the present study is to examine the role of Kcnj10 in contributing to the basolateral K conductance in the cortical thick ascending limb (cTAL) using Kcnj10+/+ and ‐/‐ mice. The patch‐clamp studies detected a 40 pS and a 80 pS K channel in the basolateral membrane of the cTAL. Moreover, the probability of finding the 40 pS K was significantly higher in the upper part of the cTAL than in the lower portion. Immunostaining showed that Kcnj10 was expressed mainly in the basolateral membrane of the cTAL close to glomerulus but not in all portion of cTAL. The disruption of Kcnj10 completely eliminated the 40 pS K channel but not the 80 pS K channel, suggesting the role of Kcnj10 in forming the 40 pS K channel of the cTAL. Also, the disruption of Kcnj10 increased the probability of finding the 80 pS K channel in the cTAL. Because the channel open probability of the 80 pS K channel in the KO mice was similar to those of WT mice, this suggests that the disruption of Kcnj10‐induced increase in the 80 pS K channel is mainly achieved by increasing K channel number in the plasma membrane. The whole cell recording further showed that K reversal potential measured with 5 mM K in the bath and 140 mM K in the pipette was the same in the WT and KO mice. Moreover, Western blot and immunostaining show that the disruption of Kcnj10 did not affect the expression of NKCC2. We conclude that KCNJ10 is expressed in the basolateral membrane of cTAL and that the disruption of Kcnj10 has no significant effect on the membrane potential of the TAL and NKCC2 expression.