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This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/F1033    most recent 00086.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science 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 ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Pihakaski-Maunsbach, K. Articles by Maunsbach, A. B. Search for Related Content PubMed PubMed Citation Articles by Pihakaski-Maunsbach, K. Articles by Maunsbach, A. B.

Locations, abundances, and possible functions of FXYD ion transport regulators in rat renal medulla

¹The Water and Salt Research Center, ²Department of Cell Biology, Institute of Anatomy, ³Institute of Medical Biochemistry, and ⁴Department of Clinical Physiology, University of Aarhus, Aarhus, Denmark; and ⁵Department of Biological Chemistry, Weizmann Institute of Science, Rehovoth, Israel

Submitted 14 March 2006 ; accepted in final form 31 May 2006

The -subunit of Na-K-ATPase (FXYD2) and corticosteroid hormone-induced factor (CHIF; FXYD4) are considered pump regulators in kidney tubules. The aim of this study was to expand the information about their locations in the kidney medulla and to evaluate their importance for electrolyte excretion in an animal model. The cellular and subcellular locations and abundances of and CHIF in the medulla of control and sodium-depleted rats were analyzed by immunofluorescence and immunoelectron microscopy and semiquantitative Western blotting. The results showed that antibodies against the -subunit COOH terminus and splice variant _a, but not splice variant _b, labeled intercalated cells, but not principal cells, in the initial part of the inner medullary collecting duct (IMCD1). In subsequent segments (IMCD2 and IMCD3), all principal cells exhibited distinct basolateral labeling for both the -subunit COOH terminus, splice variant _a, and CHIF. Splice variant _b was abundant in the inner stripe of the outer medulla but absent in the inner medulla (IM). Double labeling by high-resolution immunoelectron microscopy showed close structural association between CHIF and the Na-K-ATPase ₁-subunit in basolateral membranes. The present observations provide new information about the cellular and subcellular locations of and CHIF in the renal medulla and show a new variant in the IM. Extensive NaCl depletion did not induce significant changes in the locations or abundances of the -subunit COOH terminus and CHIF in different kidney zones. We conclude that the unchanged levels of these two FXYD proteins suggest that they are not primary determinants for urine electrolyte composition during NaCl depletion.

Na-K-ATPase -subunit; CHIF; kidney medulla

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