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Please use this identifier to cite or link to this item: http://ir.fmu.ac.jp/dspace/handle/123456789/354

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Title: Effects of a high-sodium diet on renal tubule Ca2+ transporter and claudin expression in Wistar-Kyoto rats
Authors: Yatabe, Midori Sasaki
Yatabe, Junichi
Takano, Kozue
Murakami, Yuta
Sakuta, Rina
Abe, Sadahiko
Sanada, Hironobu
Kimura, Junko
Watanabe, Tsuyoshi
Affiliation: 薬理学講座
Source title: BMC nephrology
Volume: 13
Start page: 160
Issue Date: 2-Dec-2012
Abstract: Background: Urinary Ca^{2+} excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca^{2+} transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca^{2+} loss. Methods: Eight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca^{2+} pump (PCMA1b), Ca^{2+} channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and −19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry. Results: Fractional excretion of Ca^{2+} increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and −19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively. Conclusions: Chronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca^{2+}. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca^{2+} reabsorption in this segment. The concerted upregulation of more distal Ca^{2+}-transporting molecules may be a physiological response to curtail the loss of Ca^{2+}, although the magnitude of compensation does not seem adequate to bring the urinary Ca^{2+} excretion down to that of the normal-diet group.
Publisher: BioMed Central Ltd.
language: eng
URI: http://ir.fmu.ac.jp/dspace/handle/123456789/354
Full text URL: http://ir.fmu.ac.jp/dspace/bitstream/123456789/354/1/1471-2369-13-160.pdf
ISSN: 1471-2369
DOI: 10.1186/1471-2369-13-160
PubMed ID: 23199000
Other version: http://dx.doi.org/10.1186/1471-2369-13-160
Rights: © 2012 Yatabe et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Rights: http://creativecommons.org/licenses/by/2.0
Appears in Collections:a10 学術雑誌論文等 = Journal Article

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