UPREGULATION OF CLAUDIN-4 IN THE KIDNEY OF DAHL SALT-SENSITIVE RATS
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Gheun-Ho | - |
dc.contributor.author | Jo, Chor Ho | - |
dc.contributor.author | Kim, Sua | - |
dc.contributor.author | Oh, Il Hwan | - |
dc.contributor.author | Park, Joon-Sung | - |
dc.date.accessioned | 2021-08-03T06:09:14Z | - |
dc.date.available | 2021-08-03T06:09:14Z | - |
dc.date.created | 2021-06-17 | - |
dc.date.issued | 2016-09-24 | - |
dc.identifier.issn | 0263-6352 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/35487 | - |
dc.description.abstract | Objective: Claudins are tight junction proteins that regulate paracellular permeability of renal epithelia, and renal paracellular sodium chloride permeability may be essential to salt homeostasis and blood pressure control. A previous study has shown that the collecting duct-specific claudin-4 knockout animals develop hypotension due to profound renal wasting of chloride. This study was undertaken to investigate whether claudins have a role in the hypertension of Dahl salt-sensitive (DS) rats. Design and Method: Male DS and Dahl salt-resistant (DR) rats, 6 of each, were maintained on an 8% NaCl-containing rodent diet for 4 weeks. Systolic blood pressure (SBP) and plasma and urine electrolytes were weekly measured. At the end of animal experiment, kidneys were harvested for immunoblotting and quantitative PCR analysis of tight junction proteins including claudin-2, claudin-4, claudin-7, claudin-8, occludin, and ZO-1. Results: SBP was significantly higher in DS than in DR rats at the 1st to 4th week of the animal experiment. At the 1st and 2nd week, urine sodium and chloride excretion were significantly reduced in DS as compared with DR rats. At the 2nd week, DS rats had lower concentrations of plasma sodium and chloride than DR rats. The body weight measured at the end of animal experiment was lower in DS than in DR rats. In the kidney, claudin-4 protein and mRNA were significantly increased in DS as compared with DR rats. On the other hand, occludin protein and mRNA were significantly decreased in DS as compared with DR rats. The expressions of claudin-2, claudin-7, and claudin-8 were not significantly different between the two groups. Conclusions: In DS rats, salt-sensitive hypertension was associated with differential changes in renal tight junction protein expression. Upregulation of claudin-4 might increase paracellular sodium chloride transport in the kidney, resulting in impaired pressure natriuresis in DS rats. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | Hypertension Seoul 2016 조직위원회 | - |
dc.title | UPREGULATION OF CLAUDIN-4 IN THE KIDNEY OF DAHL SALT-SENSITIVE RATS | - |
dc.type | Conference | - |
dc.contributor.affiliatedAuthor | Kim, Gheun-Ho | - |
dc.contributor.affiliatedAuthor | Park, Joon-Sung | - |
dc.identifier.wosid | 000440372401233 | - |
dc.identifier.bibliographicCitation | Hypertension Seoul 2016: The 26th Scientific Meeting of the International Society of Hypertension, pp.E236 | - |
dc.relation.isPartOf | Hypertension Seoul 2016: The 26th Scientific Meeting of the International Society of Hypertension | - |
dc.relation.isPartOf | ISH 2016 Abstract Book Supplement 1 | - |
dc.citation.title | Hypertension Seoul 2016: The 26th Scientific Meeting of the International Society of Hypertension | - |
dc.citation.startPage | E236 | - |
dc.citation.endPage | E236 | - |
dc.citation.conferencePlace | KO | - |
dc.citation.conferencePlace | 서울 코엑스 | - |
dc.citation.conferenceDate | 2016-09-24 | - |
dc.type.rims | CONF | - |
dc.description.journalClass | 1 | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
222, Wangsimni-ro, Seongdong-gu, Seoul, 04763, Korea+82-2-2220-1365
COPYRIGHT © 2021 HANYANG UNIVERSITY.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.