Adenosine stimulates the basolateral 50 pS K channels in the thick ascending limb of the rat kidney

Gu, Ruimin; Wang, Jing; Zhang, Yunhong; Li, Wennan; Xu, Ying; Shan, Hongli; Wang, Wenhui; Yang, Baofeng

doi:10.1152/ajprenal.00008.2007

Cited by 13 publications

(19 citation statements)

References 32 publications

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“…Patch-clamp experiments have identified two types of K + channels, a 40-50 pS inwardly-rectifying and an 80-150 pS Na + and Cl - activated, in the basolateral membrane of the mouse TAL [7,21,23]. We now confirmed that the same two types of K + channels are also expressed in the basolateral membrane of rat TAL.…”

Section: Discussionsupporting

confidence: 74%

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Vasopressin-induced stimulation of the Na+-activated K+ channels is responsible for maintaining the basolateral K+ conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome

Fan

Wang

Zhang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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The renal phenotype of EAST syndrome, a disease caused by the loss-of-function-mutations of Kcnj10 (Kir4.1), is a reminiscence of Gitelman's syndrome characterized by the defective function in the distal convoluted tubule (DCT). The aim of the present study is to test whether antidiuretic hormone (vasopressin)-induced stimulation of the Na+-activated 80-150 pS K+ channel is responsible for compensating the lost function of Kcnj10 in the thick ascending limb (TAL) of subjects with EAST syndrome. Immunostaining and Western blot showed that the expression of aquaporin 2 (AQP2) was significantly higher in Kcnj10-/- mice than those of WT littermates, suggesting that the disruption of Kcnj10 stimulates vasopressin response in the kidney. The role of vasopressin in stimulating the basolateral K+ conductance of the TAL was strongly indicated by the finding that the application of arginine-vasopressin (AVP) hyperpolarized the membrane in the TAL of Kcnj10-/- mice. Application of AVP significantly stimulated the 80-150 pS K+ channel in the TAL and this effect was blocked by tolvaptan (V2 receptor antagonist) or by inhibiting PKA. Moreover, the water restriction for 24 hours significantly increased the probability of finding the 80-150 pS K+ channel and the K+ channel open probability in the TAL. The application of a membrane permeable cAMP analog also mimicked the effect of AVP and activated this K+ channel, suggesting that cAMP-PKA pathway stimulates the 80-150 pS K+ channels. The role of the basolateral K+ conductance in maintaining transcellular Cl- transport is further suggested by the finding that the inhibition of basolateral K+ channels significantly diminished the AVP-induced stimulation of the basolateral 10 pS Cl- channels. We conclude that vasopressin stimulates the 80-150 pS K+ channel in the TAL via a cAMP-dependent mechanism. The vasopressin-induced stimulation of K+ channels is responsible for compensating lost function of Kcnj10 thereby rescuing the basolateral K+ conductance which is essential for the transport function in the TAL.

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Section: Discussionsupporting

confidence: 74%

“…Because the present study is focused on testing the effect of vasopressin on the 80-150 pS K + channel, we did not examine the effect of ADH on the 40-50 pS K channel which is known to be activated by cAMP pathway [7]. Fig.…”

Section: Resultsmentioning

confidence: 99%

Vasopressin-induced stimulation of the Na+-activated K+ channels is responsible for maintaining the basolateral K+ conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome

Fan

Wang

Zhang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…However, the authors have been unable to ascertain to which specific K ϩ channel gene families these K ϩ channels belong. Unclassified channels are reported in the basolateral membrane of PT cells (7, 32, 33, 51-53, 62, 63, 97, 111, 125), TAL cells (24,39,40), DCT cells (123), and CNT/CD cells (36,(47)(48)(49)82).…”

Section: Kcnj Gene Family Members In the Nephronmentioning

confidence: 99%

Basolateral membrane K⁺channels in renal epithelial cells

Hamilton

Devor

2012

American Journal of Physiology-Renal Physiology

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The major function of epithelial tissues is to maintain proper ion, solute, and water homeostasis. The tubule of the renal nephron has an amazingly simple structure, lined by epithelial cells, yet the segments (i.e., proximal tubule vs. collecting duct) of the nephron have unique transport functions. The functional differences are because epithelial cells are polarized and thus possess different patterns (distributions) of membrane transport proteins in the apical and basolateral membranes of the cell. K(+) channels play critical roles in normal physiology. Over 90 different genes for K(+) channels have been identified in the human genome. Epithelial K(+) channels can be located within either or both the apical and basolateral membranes of the cell. One of the primary functions of basolateral K(+) channels is to recycle K(+) across the basolateral membrane for proper function of the Na(+)-K(+)-ATPase, among other functions. Mutations of these channels can cause significant disease. The focus of this review is to provide an overview of the basolateral K(+) channels of the nephron, providing potential physiological functions and pathophysiology of these channels, where appropriate. We have taken a "K(+) channel gene family" approach in presenting the representative basolateral K(+) channels of the nephron. The basolateral K(+) channels of the renal epithelia are represented by members of the KCNK, KCNJ, KCNQ, KCNE, and SLO gene families.

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“…Moreover, the finding that the disruption of Kcnj10 alone completely eliminated the 40-pS K channel in the distal convoluted tubule (DCT) strongly suggests that Kir4.1 is a pore-forming component of the Kir4.1/5.1 heterotetramer. We and others previously detected an inwardly rectifying K channel in the basolateral membrane of the cortical thick ascending limb (cTAL) of both rat and CD1 mouse kidney with similar biophysical properties to those of the 40-pS K channel (5,6,14). However, it is not known whether a K channel of the same type is present in the cTAL of C57bl/6 mice.…”

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confidence: 98%

KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb

Zhang

Li-jun

et al. 2015

American Journal of Physiology-Renal Physiology

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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.

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Adenosine stimulates the basolateral 50 pS K channels in the thick ascending limb of the rat kidney

Cited by 13 publications

References 32 publications

Vasopressin-induced stimulation of the Na+-activated K+ channels is responsible for maintaining the basolateral K+ conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome

Vasopressin-induced stimulation of the Na+-activated K+ channels is responsible for maintaining the basolateral K+ conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome

Basolateral membrane K⁺channels in renal epithelial cells

KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb

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Adenosine stimulates the basolateral 50 pS K channels in the thick ascending limb of the rat kidney

Cited by 13 publications

References 32 publications

Vasopressin-induced stimulation of the Na+-activated K+ channels is responsible for maintaining the basolateral K+ conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome

Vasopressin-induced stimulation of the Na+-activated K+ channels is responsible for maintaining the basolateral K+ conductance of the thick ascending limb (TAL) in EAST/SeSAME syndrome

Basolateral membrane K+channels in renal epithelial cells

KCNJ10 (Kir4.1) is expressed in the basolateral membrane of the cortical thick ascending limb

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Basolateral membrane K⁺channels in renal epithelial cells