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Angiotensin II and ...
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Jönsson, SofiaUppsala universitet,Institutionen för medicinsk cellbiologi,Michael Hultström
(författare)
Angiotensin II and salt-induced decompensation in Balb/CJ mice is aggravated by fluid retention related to low oxidative stress
- Artikel/kapitelEngelska2019
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American Physiological Society,2019
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:umu-159399
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-159399URI
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https://doi.org/10.1152/ajprenal.00483.2018DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-379717URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Balb/CJ mice are more sensitive to treatment with angiotensin II (ANG II) and high-salt diet compared with C57BL/6J mice. Together with higher mortality, they develop edema, signs of heart failure, and acute kidney injury. The aim of the present study was to identify differences in renal gene regulation that may affect kidney function and fluid balance, which could contribute to decompensation in Balb/CJ mice after ANG II + salt treatment. Male Balb/CJ and C57BL/6J mice were divided into the following five different treatment groups: control, ANG II, salt, ANG II + salt. and ANG II + salt + N-acetylcysteine. Gene expression microarrays were used to explore differential gene expression after treatment and between the strains. Published data from the Mouse Genome Database were used to identify the associated genomic differences. The glomerular filtration rate (GFR) was measured using inulin clearance, and fluid balance was measured using metabolic cages. Gene ontology enrichment analysis of gene expression microarrays identified glutathione transferase (antioxidant system) as highly enriched among differentially expressed genes. Balb/CJ mice had similar GFR compared with C57BL/6J mice but excreted less Na+ and water, although net fluid and electrolyte balance did not differ, suggesting that Balb/CJ mice may be inherently more prone to decompensation. Interestingly, C57BL/6J mice had higher urinary oxidative stress despite their relative protection from decompensation. In addition, treatment with the antioxidant N-acetylcysteine decreased oxidative stress in C57BL/6J mice, reduced urine excretion, and increased mortality. Balb/CJ mice are more sensitive than C57BL/6J to ANG II + salt, in part mediated by lower oxidative stress, which favors fluid and Na+ retention.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Agic, Mediha BecriovicUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)medbe300
(författare)
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Isackson, HenrikUppsala universitet,Institutionen för medicinsk cellbiologi,Kardiologi,UCR
(författare)
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Tveitarås, Maria K.Department of Biomedicine, University of Bergen, Bergen, Norway
(författare)
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Skogstrand, TrudeDepartment of Biomedicine, University of Bergen, Bergen, Norway
(författare)
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Narfström, FredrikUppsala universitet,Institutionen för medicinsk cellbiologi
(författare)
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Karlsen, Tine, VDepartment of Biomedicine, University of Bergen, Bergen, Norway
(författare)
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Lidén, ÅsaDepartment of Biomedicine, University of Bergen, Bergen, Norway
(författare)
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Leh, SabineDepartment of Pathology, Haukeland University Hospital Bergen, Department of Clinical Medicine, University of Bergen, Bergen, Norway
(författare)
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Ericsson, MadeleneUmeå universitet,Fysiologisk kemi,Department of Medical Biosciences, umeå University, Umeå, Sweden(Swepub:umu)maer0239
(författare)
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Nilsson, Stefan K.,1979-Umeå universitet,Fysiologisk kemi,Department of Medical Biosciences, umeå University, Umeå, Sweden(Swepub:umu)nist6501
(författare)
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Reed, Rolf K.Department of Biomedicine, University of Bergen, Bergen, and Centre for Cancer Biomarkers (CCBIO), University of Bergen, Norway
(författare)
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Hultström, Michael,1978-Uppsala universitet,Institutionen för medicinsk cellbiologi,Anestesiologi och intensivvård(Swepub:uu)mihul498
(författare)
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Uppsala universitetInstitutionen för medicinsk cellbiologi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:American Journal of Physiology - Renal Physiology: American Physiological Society316:5, s. F914-F9331931-857X1522-1466
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Jönsson, Sofia
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Agic, Mediha Bec ...
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Isackson, Henrik
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Tveitarås, Maria ...
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Skogstrand, Trud ...
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Narfström, Fredr ...
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Karlsen, Tine, V
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Lidén, Åsa
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Leh, Sabine
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Ericsson, Madele ...
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Nilsson, Stefan ...
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Reed, Rolf K.
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Hultström, Micha ...
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