ArticleJournal of the American Society of Nephrology : JASN2017
The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 104 citations in OpenAlex.
- Reduced Expression of Magnesium Transport Proteins in the Distal Convoluted Tubule of Clcnkb-Deficient Mice May Explain Urinary Magnesium Wasting in Classical Bartter Syndrome.Acta physiologica (Oxford, England) · 2026Article
- Chloride at the spotlight-but not alone: towards a multi-ionic diuretic strategy.Clinical kidney journal · 2026Review
- Stimulation of basolateral calcium-sensing receptor inhibits Kir4.1/Kir5.1 in the mouse distal convoluted tubule.American journal of physiology. Renal physiology · 2026Article
- Nitric oxide mediates ET-1-induced-inhibition of NPPB-sensitive ClThe Journal of biological chemistry · 2026Article
- Predicting In-Hospital Mortality in Intensive Care Unit Patients Using Causal SurvivalNet With Serum Chloride and Other Causal Factors: Cross-Country Study.Journal of medical Internet research · 2025Article
- Intercalated Cell ClC-K2 Channel Contributes to Systemic ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- ClC-Kb pore mutation disrupts glycosylation and triggers distal tubular remodeling.JCI insight · 2024Article
- mTORc2 in Distal Convoluted Tubule and Renal K + Excretion during High Dietary K + Intake.Journal of the American Society of Nephrology : JASN · 2024Article
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Low potassium activation of proximal mTOR/AKT signaling is mediated by Kir4.2.Nature communications · 2024Article
- Review
- Novel functions of the anion exchanger AE4 (SLC4A9).Pflugers Archiv : European journal of physiology · 2024Review
- Effect of low sodium and high potassium diet on lowering blood pressure and cardiovascular events.Clinical hypertension · 2024Review
- Mechanisms and physiological relevance of acid-base exchange in functional units of the kidney.PeerJ · 2024Review
- ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024Article
- Expanding Genotype-Phenotype Correlation ofInternational journal of molecular sciences · 2023Article
- Gitelman Syndrome: A Case Report.Cureus · 2023Article
- Small Molecules Targeting Kidney ClC-K Chloride Channels: Applications in Rare Tubulopathies and Common Cardiovascular Diseases.Biomolecules · 2023Review
- Review
- Inhibitory effect of S-nitroso-N-acetylpenicillamine on the basolateral 10-pS Cl- channel in thick ascending limb.PloS one · 2023Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chloride transport by the renal tubule is critical for blood pressure (BP), acid-base, and potassium homeostasis. Chloride uptake from the urinary fluid is mediated by various apical transporters, whereas basolateral chloride exit is thought to be mediated by ClC-Ka/K1 and ClC-Kb/K2, two chloride channels from the ClC family, or by KCl cotransporters from the SLC12 gene family. Nevertheless, the localization and role of ClC-K channels is not fully resolved. Because inactivating mutations in ClC-Kb/K2 cause Bartter syndrome, a disease that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a critical role in salt handling by the thick ascending limb. To dissect the role of this channel in detail, we generated a mouse model with a targeted disruption of the murine ortholog ClC-K2. Mutant mice developed a Bartter syndrome phenotype, characterized by renal salt loss, marked hypokalemia, and metabolic alkalosis. Patch-clamp analysis of tubules isolated from knockout (KO) mice suggested that ClC-K2 is the main basolateral chloride channel in the thick ascending limb and in the aldosterone-sensitive distal nephron. Accordingly, ClC-K2 KO mice did not exhibit the natriuretic response to furosemide and exhibited a severely blunted response to thiazide. We conclude that ClC-Kb/K2 is critical for salt absorption not only by the thick ascending limb, but also by the distal convoluted tubule.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.