The disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct.

The disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct. Am J Physiol Renal Physiol. 2016 Feb 17;:ajprenal.00584.2015 Authors: Su XT, Zhang C, Wang L, Gu R, Lin DH, Wang WH Abstract Kcnj10 encodes the inwardly rectifying K(+) channel 4.1 (Kir4.1) and is expressed in the basolateral membrane of late TAL, DCT, CNT and CCD. In the present study, we perform experiments in p9 WT and Kcnj10(-/-) mice to examine the role of Kir.4.1 in contributing to the basolateral K(+) conductance in the CNT and CCD, and to investigate whether disruption of Kir4.1 up-regulates ENaC expression. Immunostaining shows that Kir4.1 and Kir5.1 are expressed in the basolateral membrane of CNT and CCD. The patch-clamp studies detect three types of K(+) channels (23 pS, 40 pS and 60 pS) in the basolateral membrane of the late CNT and initial CCD in the WT mice. However, only 23 pS and 60 pS K(+) channels but not the 40 pS K(+) channel were detected in Kcnj10(-/-) mice, suggesting that Kir.4.1 is a key component of the 40 pS K(+) channel in the CNT/CCD. Moreover, the depletion of Kir.4.1 did not increase the probability of finding the 23 pS and 60 pS K(+) channel in the CNT/CCD. We next used the perforated whole cell recording to measure the K(+) reversal voltage in the CNT/CCD as an index of the cell membrane potential. Under control conditions, the K(+) reversal potential was -69 mV in the WT mice and it was -61 mV in Kcnj10(-/-)...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research