title: KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb.
abstract: The aim of the present study is to examine the role of Kcnj10 (Kir.4.1) in contributing to the basolateral K conductance in the cortical thick ascending limb (cTAL) using Kcnj10(+/+) wild-type (WT) and Kcnj10(-/-) knockout (KO) mice. The patch-clamp experiments detected a 40- and an 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 late part of the cTAL close to the distal convoluted tubule than those in the initial part. Immunostaining showed that Kcnj10 staining was detected in the basolateral membrane of the cTAL but the expression was not uniformly distributed. 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, especially in the late part of the cTAL. Because the channel open probability of the 80-pS K channel in KO was similar to those of WT mice, the increase in the 80-pS K channel may be achieved by increasing K channel number. 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 showed that the disruption of Kcnj10 did not affect the expression of Na-K-Cl cotransporter 2 (NKCC2). We conclude that Kir.4.1 is expressed in the basolateral membrane of cTAL and that the disruption of Kir.4.1 has no significant effect on the membrane potential of the cTAL and NKCC2 expression.
authors.affiliation: Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou, Jiangsu, China; and Department of Pharmacology, New York Medical College, Valhalla, New York.
authors.forename: Chengbiao
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Pharmacology, New York Medical College, Valhalla, New York.
authors.forename: Lijun
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Pharmacology, New York Medical College, Valhalla, New York.
authors.forename: Xiao-Tong
authors.initials: XT
authors.lastname: Su
authors.affiliation: Department of Pharmacology, New York Medical College, Valhalla, New York.
authors.forename: Dao-Hong
authors.initials: DH
authors.lastname: Lin
authors.affiliation: Department of Pharmacology, New York Medical College, Valhalla, New York wenhui_wang@nymc.edu.
authors.forename: Wen-Hui
authors.initials: WH
authors.lastname: Wang
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D005121:Extremities; D017136:Ion Transport / Q000502:physiology; D007686:Kidney Tubules, Distal / Q000378:metabolism*; D008564:Membrane Potentials / Q000502:physiology*; D018345:Mice, Knockout; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D064466:Solute Carrier Family 12, Member 1 / Q000378:metabolism; D000098854:Kcnj10 Channel
chemical_list: D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying; C578715:Slc12a1 protein, mouse; D064466:Solute Carrier Family 12, Member 1; D012964:Sodium
keywords: EAST/SeSAME syndrome; Kir.4.1; Kir5.1; NKCC2
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