ReviewCurrent opinion in nephrology and hypertension2023
The K-Cl cotransporter-3 in the mammalian kidney.
Review in Current opinion in nephrology and hypertension, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Exploring the Role of the SLC12A Cation-Coupled Chloride Cotransporters in the Cardiovascular System.Cells · 2026Review
- Sheep erythrocyte potassium locus highlights MYADM family regulation of electroneutral potassium chloride cotransporters (KCC).BMC genomics · 2026Article
- Novel functions of the anion exchanger AE4 (SLC4A9).Pflugers Archiv : European journal of physiology · 2024Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
purpose of reviewWe recently localized a new K-Cl cotransporters-3 (KCC3) transporter to the apical membrane of type-B intercalated cells. This gives us an opportunity to revisit the roles of the KCC3 in kidney and integrate the new findings to our current knowledge of the biology of the bicarbonate secreting cells. RECENT
findingsHere, we review the basic properties of the K-Cl cotransporter with a particular attention to the responsiveness of the transporter to cell swelling. We summarize what is already known about KCC3b and discuss new information gained from our localizing of KCC3a in type-B intercalated cells. We integrate the physiology of KCC3a with the main function of the type-B cell, that is, bicarbonate secretion through the well characterized apical Cl-/HCO3- exchanger and the basolateral Na-HCO3 cotransporter. SUMMARY: Both KCC3b and KCC3a seem to be needed for maintaining cell volume during enhanced inward cotransport of Na-glucose in proximal tubule and Na-HCO3 in intercalated cells. In addition, apical KCC3a might couple to pendrin function to recycle Cl-, particularly in conditions of low salt diet and therefore low Cl- delivery to the distal tubule. This function is critical in alkalemia, and KCC3a function in the pendrin-expressing cells may contribute to the K+ loss which is observed in alkalemia.
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