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Am J Physiol Renal Physiol (August 15, 2001). doi:10.1152/ajprenal.0085.2001
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Articles in PresS, published online ahead of print August 15, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0085.2001
Submitted on March 13, 2001
Accepted on August 10, 2001

Organization of the mouse distal nephron: distributions of transcellular calcium and sodium transport pathways

Johannes Loffing1*, Dominique Loffing-Cueni1, Victor Valderrabano1, Lea Klausli1, Steven C Hebert2, Bernard C Rossier3, Joost G Hoenderop4, Rene J Bindels4, and Brigitte Kaissling1

1 Institute of Anatomy, University of Zurich, Zurich, Switzerland
2 Department of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA
3 Institute of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland
4 Department of Cell Physiology, University Medical Centre Nijmegen, Nijmegen, Netherlands

* To whom correspondence should be addressed. E-mail: jloffing{at}anatom.unizh.ch.

Genetically modified mice are used as models for studying physiology and pathophysiology of electrolyte metabolism, yet, data on the organization of Na+ and Ca2+ transporting proteins along the mouse distal nephron are incomplete. We describe by immunohistochemistry in mouse kidney cortex the sequential distributions of the thiazide-sensitive Na+-Cl--cotransporter (NCC), the amiloride-sensitive epithelial Na+ channel (ENaC), the epithelial Ca2+ channel 1 (ECaC1), the plasma membrane Ca2+-ATPase (PMCA), the Na+-Ca2+ exchanger (NCX), and the cytoplasmic calcium-binding proteins calbindin D28k (CB) and parvalbumin (PV). NCC characterized the distal convoluted tubule (DCT). In the second half of the DCT, in DCT2, NCC was co-expressed with ENaC. The latter extended all along the connecting tubule (CNT) and the cortical collecting duct (CCD). ECaC1 was detected in DCT2 and CNT. The apical abundance of ECaC1 was high in DCT2, decreased, and changed progressively to cytoplasmic location along the CNT. Basolateral NCX and PMCA were weakly apparent in DCT1, were the most abundant in DCT2, decreased gradually along the CNT, and were undetectable in CCD. Cytoplasmic CB was barely detectable in early DCT, steeply increased to very high levels with the beginning of DCT2, and was found at intermediate levels in CNT and CCD. PV was seen at high levels in the cytoplasm and nuclei of DCT1 cells. The co-occurrence of calcium-transporting ECaC1, NCX and PMCA in the mouse DCT2 and CNT reveals the capacity of these segments for active transcellular calcium transport. Co-localization of ECaC1 with NCC and ENaC in the apical plasma membrane of mouse DCT2 cells, and of ECaC1 and ENaC in CNT cells provides a morphological basis for understanding and studying the complex interplay of Na+ and Ca2+ transport in the distal nephron of this species.




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