ArticleThe Journal of general physiology2016
Dual regulation of the native ClC-K2 chloride channel in the distal nephron by voltage and pH.
Article in The Journal of general physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- ClC-K Kidney Chloride Channels: From Structure to Pathology.Handbook of experimental pharmacology · 2024Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Bartter and Gitelman syndromes: Questions of class.Pediatric nephrology (Berlin, Germany) · 2020Review
- The Renal Physiology of Pendrin-Positive Intercalated Cells.Physiological reviews · 2020Review
- DHHC7-mediated palmitoylation of the accessory protein barttin critically regulates the functions of ClC-K chloride channels.The Journal of biological chemistry · 2020Article
- Functional Study of Novel Bartter's Syndrome Mutations in ClC-Kb and Rescue by the Accessory Subunit Barttin Toward Personalized Medicine.Frontiers in pharmacology · 2020Article
- α-Ketoglutarate stimulates pendrin-dependent ClAmerican journal of physiology. Renal physiology · 2018Article
- The Role of Intercalated CellJournal of the American Society of Nephrology : JASN · 2018Article
- Activation of renal ClC-K chloride channels depends on an intact N terminus of their accessory subunit barttin.The Journal of biological chemistry · 2018Article
- Renal intercalated cells and blood pressure regulation.Kidney research and clinical practice · 2017Review
- Functional severity of CLCNKB mutations correlates with phenotypes in patients with classic Bartter's syndrome.The Journal of physiology · 2017Article
- Reduced Membrane Insertion of CLC-K by V33L Barttin Results in Loss of Hearing, but Leaves Kidney Function Intact.Frontiers in physiology · 2017Article
- Alkaline activation of ClC-K2 chloride channels switches renal cells from reabsorbing to secreting.The Journal of general physiology · 2016Article
- Angiotensin II increases activity of the ClC-K2 ClThe Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ClC-K2, a member of the ClC family of Cl(-) channels and transporters, forms the major basolateral Cl(-) conductance in distal nephron epithelial cells and therefore plays a central role in renal Cl(-) absorption. However, its regulation remains largely unknown because of the fact that recombinant ClC-K2 has not yet been studied at the single-channel level. In the present study, we investigate the effects of voltage, pH, Cl(-), and Ca(2+) on native ClC-K2 in the basolateral membrane of intercalated cells from the mouse connecting tubule. The ∼10-pS channel shows a steep voltage dependence such that channel activity increases with membrane depolarization. Intracellular pH (pHi) and extracellular pH (pHo) differentially modulate the voltage dependence curve: alkaline pHi flattens the curve by causing an increase in activity at negative voltages, whereas alkaline pHo shifts the curve toward negative voltages. In addition, pHi, pHo, and extracellular Ca(2+) strongly increase activity, mainly because of an increase in the number of active channels with a comparatively minor effect on channel open probability. Furthermore, voltage alters both the number of active channels and their open probability, whereas intracellular Cl(-) has little influence. We propose that changes in the number of active channels correspond to them entering or leaving an inactivated state, whereas modulation of open probability corresponds to common gating by these channels. We suggest that pH, through the combined effects of pHi and pHo on ClC-K2, might be a key regulator of NaCl absorption and Cl(-)/HCO3 (-) exchange in type B intercalated cells.
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