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This Article Full Text Full Text (PDF) All Versions of this Article: 90/2/195    most recent expphysiol.2004.028886v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fowler, M. R Articles by Hunter, M. Search for Related Content PubMed PubMed Citation Articles by Fowler, M. R Articles by Hunter, M. Related Collections GI & Epithelial

¹ School of Biomedical Sciences, Worsley Building, University of Leeds, Leeds, LS2 9NQ, UK

A global and transient rise of intracellular Ca²⁺ (Ca²⁺_i) is central to the operation of pump–leak coupling in the frog early distal tubule (EDT). The endoplasmic reticulum (ER) is the site of this Ca²⁺ release and reuptake; however, it is likely that other intracellular pools, such as mitochondria, also contribute to cellular Ca²⁺ homeostasis. The present study was performed to seek evidence of mitochondrial Ca²⁺ transport in the frog EDT. Experiments were performed on isolated and permeabilized EDT segments from the frog kidney loaded with the low-affinity, Ca²⁺-sensitive fluorescent indicator, mag-fura-2. Ca²⁺ uptake in the absence of SarcoEndoplasmic Reticulum Calcium ATPase (SERCA) activity (inhibition by 2,5-di-t-butyl hydroquinone, TBQ) was evident at a bath [Ca²⁺] of 1 µM, but not at 200 nM, in the presence of ATP. This uptake was sensitive to the protonophore FCCP and the ATP-synthase inhibitor oligomycin. Ca²⁺ uptake was also stimulated by respiratory substrates; this uptake was enhanced by oligomycin and reversed by the application of FCCP. These findings provide the first evidence of mitochondrial Ca²⁺ transport in renal tubules, which appears to occur via a low-affinity pathway and which will act as a physiological Ca²⁺ buffer, protecting the cell from large increases in Ca²⁺_i.

(Received 1 September 2004; accepted after revision 8 November 2004; first published online 30 November 2004)
Corresponding author M. Hunter: School of Biomedical Sciences, Worsley Building, University of Leeds, Leeds, LS2 9NQ, UK. Email: m.hunter{at}leeds.ac.uk

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