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Changes in the sodium and potassium transporters in the course of chronic renal failure

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dc.contributor.authorKim, S.-
dc.contributor.authorHeo, N.J.-
dc.contributor.authorJung, J.Y.-
dc.contributor.authorSon, M.-J.-
dc.contributor.authorJang, H.R.-
dc.contributor.authorLee, J.W.-
dc.contributor.authorOh, Y.K.-
dc.contributor.authorNa, K.Y.-
dc.contributor.authorJoo, K.W.-
dc.contributor.authorHan, J.S.-
dc.date.accessioned2021-06-18T12:44:17Z-
dc.date.available2021-06-18T12:44:17Z-
dc.date.issued2010-07-
dc.identifier.issn1660-2137-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/46891-
dc.description.abstractBackground: In chronic renal failure (CRF), residual nephrons can increase their excretion of sodium (Na) and potassium (K). However, the mechanisms of renal Na and K regulation in late-stage CRF have not been clearly investigated. Methods: We examined altered expression of major renal Na and K transporters in Sprague-Dawley rats at 4 and 12 weeks after a 5/6 nephrectomy. Results: CRF rats were azotemic and had gradually increased levels of urinary Na and K excretion over time. At 4 weeks, the abundance of Na-K-2Cl cotransporter (NKCC2), and Na-Cl cotransporter (NCC) in CRF rats increased significantly (477 and 222% of the control, respectively). In contrast, expression of NKCC2 and NCC decreased markedly at 12 weeks (55.4 and 30.8%, respectively). Expression of epithelial Na channel-α increased throughout the whole period. The abundance of renal outer medullary K-channel (ROMK) and Na-K-ATPase did not decrease at 4 weeks, but it was reduced at 12 weeks. Conclusion: We suggest that increased urinary Na excretion in late-stage CRF may be associated with decreased expression of renal Na transporters except ENaC compared to early-stage CRF, and that increased urinary K excretion in the late stage of CRF may not be related to expression of ROMK. Copyright © 2010 S. Karger AG, Basel.-
dc.language영어-
dc.language.isoENG-
dc.publisherKARGER, ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND-
dc.titleChanges in the sodium and potassium transporters in the course of chronic renal failure-
dc.typeArticle-
dc.identifier.doi10.1159/000314542-
dc.identifier.bibliographicCitationNephron - Physiology, v.115, no.4, pp p31 - p41-
dc.description.isOpenAccessN-
dc.identifier.wosid000280462400001-
dc.identifier.scopusid2-s2.0-77951959481-
dc.citation.endPagep41-
dc.citation.number4-
dc.citation.startPagep31-
dc.citation.titleNephron - Physiology-
dc.citation.volume115-
dc.type.docTypeArticle-
dc.publisher.location스위스-
dc.subject.keywordAuthorChronic renal failure-
dc.subject.keywordAuthorMembrane transport proteins-
dc.subject.keywordAuthorPotassium-
dc.subject.keywordAuthorSodium-
dc.subject.keywordPluspotassium channel-
dc.subject.keywordPluspotassium ion-
dc.subject.keywordPlusRenal outer medullary potassium channel-
dc.subject.keywordPlussodium chloride cotransporter-
dc.subject.keywordPlussodium ion-
dc.subject.keywordPlussodium potassium chloride cotransporter-
dc.subject.keywordPlusunclassified drug-
dc.subject.keywordPlusanimal experiment-
dc.subject.keywordPlusanimal model-
dc.subject.keywordPlusanimal tissue-
dc.subject.keywordPlusarticle-
dc.subject.keywordPluschronic kidney failure-
dc.subject.keywordPluscontrolled study-
dc.subject.keywordPlushistopathology-
dc.subject.keywordPlusimmunohistochemistry-
dc.subject.keywordPlusmale-
dc.subject.keywordPlusnonhuman-
dc.subject.keywordPluspotassium excretion-
dc.subject.keywordPluspotassium transport-
dc.subject.keywordPluspriority journal-
dc.subject.keywordPlusprotein expression-
dc.subject.keywordPlusrat-
dc.subject.keywordPlussodium excretion-
dc.subject.keywordPlussodium transport-
dc.subject.keywordPlusAnimals-
dc.subject.keywordPlusEpithelial Sodium Channel-
dc.subject.keywordPlusKidney Failure, Chronic-
dc.subject.keywordPlusPotassium Channels, Inwardly Rectifying-
dc.subject.keywordPlusRats-
dc.subject.keywordPlusRats, Sprague-Dawley-
dc.subject.keywordPlusSodium Chloride Symporters-
dc.subject.keywordPlusSodium-Potassium-Chloride Symporters-
dc.subject.keywordPlusTissue Distribution-
dc.relation.journalResearchAreaUrology & Nephrology-
dc.relation.journalWebOfScienceCategoryUrology & Nephrology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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