ArticleExperimental physiology2011
Sodium-bicarbonate cotransporter NBCn1/Slc4a7 inhibits NH4Cl-mediated inward current in Xenopus oocytes.
Article in Experimental physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Understanding the Physiological Role of Electroneutral NaPharmaceuticals (Basel, Switzerland) · 2022Review
- Bicarbonate-Independent Sodium Conductance of Na/HCOCurrent issues in molecular biology · 2022Article
- 4-Aminopyridine: a pan voltage-gated potassium channel inhibitor that enhances KBritish journal of pharmacology · 2018Article
- Evidence for ammonium conductance in a mouse thick ascending limb cell line.Physiological reports · 2017Article
- The divergence, actions, roles, and relatives of sodium-coupled bicarbonate transporters.Physiological reviews · 2013Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
The electroneutral Na(+)-HCO(3)(-) cotransporter NBCn1 (SLC4A7) contributes to intracellular pH maintenance and transepithelial HCO(3)(-) movement. In this study, we expressed NBCn1 in Xenopus oocytes and examined the effect of NBCn1 on oocyte NH(4)(+) transport by analysing changes in membrane potential, current and intracellular pH mediated by NH(4)Cl. In the presence of HCO(3)(-)/CO(2), applying NH(4)Cl (20 mm) produced intracellular acidification of oocytes. The acidification was faster in oocytes expressing NBCn1 than in control oocytes injected with water; however, NH(4)Cl-mediated membrane depolarization was smaller in oocytes expressing NBCn1. In HCO(3)(-)/CO(2)-free solution, NH(4)Cl produced a smaller inward current in NBCn1-expressing oocytes (56% inhibition by 20 mm NH(4)Cl, measured at --60 mV), while minimally affecting intracellular acidification. The inhibition of the current by NBCn1 was unaffected when BaCl(2) replaced KCl. Current-voltage relationships showed a positive and nearly linear relationship between NH(4)Cl-mediated current and voltage, which was markedly reduced by NBCn1. Large basal currents (before NH(4)Cl exposure) were produced in NBCn1-expressing oocytes owing to the previously characterized channel-like activity of NBCn1. Inhibiting this channel-like activity by Na(+) removal abolished the inhibitory effect of NBCn1 on NH(4)Cl-mediated currents. The currents were progressively reduced over 72-120 h after NBCn1 cRNA injection, during which the channel-like activity was high. These results indicate that NBCn1 stimulates NH(4)(+) transport by its Na(+)-HCO(3)(-) cotransport activity, while reducing NH(4)(+) conductance by its channel-like activity.
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