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Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure

We aimed to examine the effects of angiotensin II AT(1) receptor blocker on the expression of major renal sodium transporters and aquaporin-2 (AQP2) in rats with chronic renal failure (CRF). During 2 wks after 5/6 nephrectomy or sham operation, both CRF rats (n=10) and sham-operated control rats (n=...

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Autores principales: Kim, Eun-Jung, Jung, Yong-Wuk, Kwon, Tae-Hwan
Formato: Texto
Lenguaje:English
Publicado: The Korean Academy of Medical Sciences 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808601/
https://www.ncbi.nlm.nih.gov/pubmed/15831996
http://dx.doi.org/10.3346/jkms.2005.20.2.248
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author Kim, Eun-Jung
Jung, Yong-Wuk
Kwon, Tae-Hwan
author_facet Kim, Eun-Jung
Jung, Yong-Wuk
Kwon, Tae-Hwan
author_sort Kim, Eun-Jung
collection PubMed
description We aimed to examine the effects of angiotensin II AT(1) receptor blocker on the expression of major renal sodium transporters and aquaporin-2 (AQP2) in rats with chronic renal failure (CRF). During 2 wks after 5/6 nephrectomy or sham operation, both CRF rats (n=10) and sham-operated control rats (n=7) received a fixed amount of low sodium diet and had free access to water. CRF rats (n=10) were divided into two groups which were either candesartan-treated (CRF-C, n=4) or vehicletreated (CRF-V, n=6). Both CRF-C and CRF-V demonstrated azotemia, decreased GFR, polyuria, and decreased urine osmolality compared with sham-operated rats. When compared with CRF-V, CRF-C was associated with significantly higher BUN levels and lower remnant kidney weight. Semiquantitative immunoblotting demonstrated decreased AQP2 expression in both CRF-C (54% of control levels) and CRF-V (57%), whereas BSC-1 expression was increased in both CRF groups. Particularly, CRF-C was associated with higher BSC-1 expression (611%) compared with CRF-V (289%). In contrast, the expression of NHE3 (25%) and TSC (27%) was decreased in CRF-C, whereas no changes were observed in CRF-V. In conclusion, 1) candesartan treatment in an early phase of CRF is associated with decreased renal hypertrophy and increased BUN level; 2) decreased AQP2 level in CRF is likely to play a role in the decreased urine concentration, and the downregulation is not altered in response to candesartan treatment; 3) candesartan treatment decreases NHE3 and TSC expression; and 4) an increase of BSC-1 is prominent in candesartan-treated CRF rats, which could be associated with the increased delivery of sodium and water to the thick ascending limb.
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spelling pubmed-28086012010-01-20 Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure Kim, Eun-Jung Jung, Yong-Wuk Kwon, Tae-Hwan J Korean Med Sci Original Article We aimed to examine the effects of angiotensin II AT(1) receptor blocker on the expression of major renal sodium transporters and aquaporin-2 (AQP2) in rats with chronic renal failure (CRF). During 2 wks after 5/6 nephrectomy or sham operation, both CRF rats (n=10) and sham-operated control rats (n=7) received a fixed amount of low sodium diet and had free access to water. CRF rats (n=10) were divided into two groups which were either candesartan-treated (CRF-C, n=4) or vehicletreated (CRF-V, n=6). Both CRF-C and CRF-V demonstrated azotemia, decreased GFR, polyuria, and decreased urine osmolality compared with sham-operated rats. When compared with CRF-V, CRF-C was associated with significantly higher BUN levels and lower remnant kidney weight. Semiquantitative immunoblotting demonstrated decreased AQP2 expression in both CRF-C (54% of control levels) and CRF-V (57%), whereas BSC-1 expression was increased in both CRF groups. Particularly, CRF-C was associated with higher BSC-1 expression (611%) compared with CRF-V (289%). In contrast, the expression of NHE3 (25%) and TSC (27%) was decreased in CRF-C, whereas no changes were observed in CRF-V. In conclusion, 1) candesartan treatment in an early phase of CRF is associated with decreased renal hypertrophy and increased BUN level; 2) decreased AQP2 level in CRF is likely to play a role in the decreased urine concentration, and the downregulation is not altered in response to candesartan treatment; 3) candesartan treatment decreases NHE3 and TSC expression; and 4) an increase of BSC-1 is prominent in candesartan-treated CRF rats, which could be associated with the increased delivery of sodium and water to the thick ascending limb. The Korean Academy of Medical Sciences 2005-04 2005-04-30 /pmc/articles/PMC2808601/ /pubmed/15831996 http://dx.doi.org/10.3346/jkms.2005.20.2.248 Text en Copyright © 2005 The Korean Academy of Medical Sciences http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Kim, Eun-Jung
Jung, Yong-Wuk
Kwon, Tae-Hwan
Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure
title Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure
title_full Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure
title_fullStr Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure
title_full_unstemmed Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure
title_short Angiotensin II AT(1) Receptor Blockade Changes Expression of Renal Sodium Transporters in Rats with Chronic Renal Failure
title_sort angiotensin ii at(1) receptor blockade changes expression of renal sodium transporters in rats with chronic renal failure
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808601/
https://www.ncbi.nlm.nih.gov/pubmed/15831996
http://dx.doi.org/10.3346/jkms.2005.20.2.248
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