ArticleAmerican journal of physiology. Renal physiology2016
Disruption of KCNJ10 (Kir4.1) stimulates the expression of ENaC in the collecting duct.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 37 citations in OpenAlex.
- Mechanistic target of rapamycin complex-1 plays a role in inhibiting kidney KAmerican journal of physiology. Renal physiology · 2026Article
- Role of KThe American journal of pathology · 2025Article
- Effect of low sodium and high potassium diet on lowering blood pressure and cardiovascular events.Clinical hypertension · 2024Review
- Calcineurin inhibitors stimulate Kir4.1/Kir5.1 of the distal convoluted tubule to increase NaCl cotransporter.JCI insight · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Inwardly rectifying KAmerican journal of physiology. Cell physiology · 2022Review
- Crosstalk between epithelial sodium channels (ENaC) and basolateral potassium channels (KBritish journal of pharmacology · 2022Article
- The effect of high-dietary KFrontiers in physiology · 2022Article
- Dissecting the Effects of Aldosterone and Hypokalemia on the Epithelial NaFrontiers in physiology · 2022Article
- EAST/SeSAME Syndrome and Beyond: The Spectrum of Kir4.1- and Kir5.1-Associated Channelopathies.Frontiers in physiology · 2022Review
- A case series of adult patients affected by EAST/SeSAME syndrome suggests more severe disease in subjects bearingIntractable & rare diseases research · 2021Article
- Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule.Journal of the American Society of Nephrology : JASN · 2020Article
- Effect of Angiotensin II on ENaC in the Distal Convoluted Tubule and in the Cortical Collecting Duct of Mineralocorticoid Receptor Deficient Mice.Journal of the American Heart Association · 2020Article
- Expression, localization, and functional properties of inwardly rectifying KAmerican journal of physiology. Renal physiology · 2020Review
- Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake.Journal of the American Society of Nephrology : JASN · 2019Article
- Potassium acts through mTOR to regulate its own secretion.JCI insight · 2019Article
- Kir4.1/Kir5.1 in the DCT plays a role in the regulation of renal KAmerican journal of physiology. Renal physiology · 2019Article
- Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter.Journal of the American Society of Nephrology : JASN · 2019Article
- Norepinephrine-Induced Stimulation of Kir4.1/Kir5.1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Potassium conservation is impaired in mice with reduced renal expression of Kir4.1.American journal of physiology. Renal physiology · 2018Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Kcnj10 encodes the inwardly rectifying K(+) channel 4.1 (Kir4.1) and is expressed in the basolateral membrane of late thick ascending limb, distal convoluted tubule (DCT), connecting tubule (CNT), and cortical collecting duct (CCD). In the present study, we perform experiments in postneonatal day 9 Kcnj10(-/-) or wild-type 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 the disruption of Kir4.1 upregulates the expression of the epithelial Na(+) channel (ENaC). Immunostaining shows that Kir4.1 is expressed in the basolateral membrane of CNT and CCD. Patch-clamp studies detect three types of K(+) channels (23, 40, and 60 pS) in the basolateral membrane of late CNT and initial CCD in wild-type (WT) mice. However, only 23- 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- 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 cell membrane potential. Under control conditions, the K(+) reversal potential was -69 mV in WT mice and -61 mV in Kcnj10(-/-) mice, suggesting that Kir4.1 partially participates in generating membrane potential in the CNT/CCD. Western blotting and immunostaining showed that the expression of ENaCβ and ENaCγ subunits from a renal medulla section of Kcnj10(-/-) mice was significantly increased compared with that of WT mice. Also, the disruption of Kir4.1 increased aquaporin 2 expression. We conclude that Kir4.1 is expressed in the CNT and CCD and partially participates in generating the cell membrane potential. Also, increased ENaC expression in medullary CD of Kcnj10(-/-) mice is a compensatory action in response to the impaired Na(+) transport in the DCT.
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