ArticleThe Journal of physiology2004
Basolateral Na+-dependent HCO3- transporter NBCn1-mediated HCO3- influx in rat medullary thick ascending limb.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 79 citations in OpenAlex.
- Molecular Basis of Rare Inherited Tubulopathies of the Kidney: A Primer for Clinicians.International journal of molecular sciences · 2026Review
- Lack of a role of NHE4 in renal ammonia metabolism.American journal of physiology. Renal physiology · 2025Article
- State of knowledge on ammonia handling by the kidney.Pflugers Archiv : European journal of physiology · 2024Review
- NHFrontiers in physiology · 2024Article
- Potential Novel Role of Membrane-Associated Carbonic Anhydrases in the Kidney.International journal of molecular sciences · 2023Review
- Dietary sodium enhances the expression of SLC4 family transporters, IRBIT, L-IRBIT, and PP1 in rat kidney: Insights into the molecular mechanism for renal sodium handling.Frontiers in physiology · 2023Article
- Understanding the Physiological Role of Electroneutral NaPharmaceuticals (Basel, Switzerland) · 2022Review
- Streptolysin S targets the sodium-bicarbonate cotransporter NBCn1 to induce inflammation and cytotoxicity in human keratinocytes during Group A Streptococcal infection.Frontiers in cellular and infection microbiology · 2022Article
- Multiple acid-base and electrolyte disturbances upregulate NBCn1, NBCn2, IRBIT and L-IRBIT in the mTAL.The Journal of physiology · 2020Article
- Deletion of the Na/HCOScientific reports · 2019Article
- Lithium increases ammonium excretion leading to altered urinary acid-base buffer composition.Journal of nephrology · 2018Article
- cAMP-dependent secretagogues stimulate the NaHCOJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2017Article
- Ammonia Transporters and Their Role in Acid-Base Balance.Physiological reviews · 2017Review
- Physiological role of NBCe2 in the regulation of electrolyte transport in the distal nephron.American journal of physiology. Renal physiology · 2015Review
- Deficient acid handling with distal RTA in the NBCe2 knockout mouse.American journal of physiology. Renal physiology · 2015Article
- Renal acid-base regulation: new insights from animal models.Pflugers Archiv : European journal of physiology · 2015Review
- Increased Epithelial Sodium Channel Activity Contributes to Hypertension Caused by Na+-HCO3- Cotransporter Electrogenic 2 Deficiency.Hypertension (Dallas, Tex. : 1979) · 2015Article
- P2X receptors trigger intracellular alkalization in isolated perfused mouse medullary thick ascending limb.Acta physiologica (Oxford, England) · 2015Article
- Thick ascending limb of the loop of Henle.Clinical journal of the American Society of Nephrology : CJASN · 2014Review
- Cation-coupled bicarbonate transporters.Comprehensive Physiology · 2014Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The electroneutral Na(+)-dependent HCO3- transporter NBCn1 is strongly expressed in the basolateral membrane of rat medullary thick ascending limb cells (mTAL) and is up-regulated during NH4(+)-induced metabolic acidosis. Here we used in vitro perfusion and BCECF video-imaging of mTAL tubules to investigate functional localization and regulation of Na(+)-dependent HCO3- influx during NH4(+)-induced metabolic acidosis. Tubule acidification was induced by removing luminal Na+ (DeltapHi: 0.88 +/- 0.11 pH units, n = 10). Subsequently the basolateral perfusion solution was changed to CO2/HCO3- buffer with and without Na+. Basolateral Na(+)-H+ exchange function was inhibited with amiloride. Na(+)-dependent HCO3- influx was determined by calculating initial base flux of Na(+)-mediated re-alkalinization. In untreated animals base flux was 8.4 +/- 0.9 pmol min(-1) mm(-1). A 2.4-fold increase of base flux to 21.8 +/- 3.2 pmol min(-1) mm(-1) was measured in NH4(+)-treated animals (11 days, n = 11). Na(+)-dependent re-alkalinization was significantly larger when compared to control animals (0.38 +/- 0.03 versus 0.22 +/- 0.02 pH units, n = 10). In addition, Na(+)-dependent HCO3- influx was of similar magnitude in chloride-free medium and also up-regulated after NH4+ loading. Na(+)-dependent HCO3- influx was not inhibited by 400 microm DIDS. A strong up-regulation of NBCn1 staining was confirmed in immunolabelling experiments. RT-PCR analysis revealed no evidence for the Na(+)-dependent HCO3- transporter NBC4 or the two Na(+)-dependent CI-/HCO3- exchangers NCBE and NDCBE. These data strongly indicate that rat mTAL tubules functionally express basolateral DIDS-insensitive NBCn1. Function and protein are strongly up-regulated during NH4(+)-induced metabolic acidosis. We suggest that NBCn1-mediated basolateral HCO3- influx is important for basolateral NH3 exit and thus NH4+ excretion by means of setting pHi to a more alkaline value.
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