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福島県立医科大学学術成果リポジトリ = Fukushima Medical University Repository >
A 医学部 = School of Medicine >
a10 学術雑誌論文等 = Journal Article >
このアイテムの引用には次の識別子を使用してください:
http://ir.fmu.ac.jp/dspace/handle/123456789/354
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| タイトル: | Effects of a high-sodium diet on renal tubule Ca2+ transporter and claudin expression in Wistar-Kyoto rats |
| 著者: | Yatabe, Midori Sasaki
Yatabe, Junichi
Takano, Kozue
Murakami, Yuta
Sakuta, Rina
Abe, Sadahiko
Sanada, Hironobu
Kimura, Junko
Watanabe, Tsuyoshi |
| 学内所属: | 薬理学講座
腎臓高血圧・糖尿病内分泌代謝内科学講座 |
| 誌名/書名: | BMC nephrology |
| 巻: | 13 |
| 開始ページ: | 160 |
| 発行日: | 2012年12月2日 |
| 抄録: | 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. |
| 出版者: | BioMed Central Ltd. |
| 本文の言語: | eng |
| このページのURI: | http://ir.fmu.ac.jp/dspace/handle/123456789/354 |
| 本文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番号: | 23199000 |
| 異版(出版者版等): | http://dx.doi.org/10.1186/1471-2369-13-160 |
| 権利情報: | © 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. |
| 権利情報: | http://creativecommons.org/licenses/by/2.0 |
| 出現コレクション: | a10 学術雑誌論文等 = Journal Article
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