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- W2022033775 abstract "To test the hypothesis that colonic Na + transport is altered in the 5/6 nephrectomized rat model of chronic renal failure (CRF), we measured Na + fluxes across distal colon from control (CON), CRF, and CRF rats treated with the angiotensin II (ANG II) receptor antagonist losartan (+LOS). We also evaluated overall fluid and Na + balance and compared colonic protein and mRNA expression profiles for electroneutral [sodium-hydrogen exchanger (NHE)] and electrogenic Na + transport [epithelial sodium channel (ENaC)] in these groups. Consistent with a 60% enhancement in colonic Na + absorption in CRF, urinary Na + excretion increased by about 50% while serum Na + homeostasis was maintained. These CRF-induced changes in Na + handling were normalized by treatment with LOS. Net Na + absorption was also stimulated in in vitro tissues from CON rats following acute serosal addition of ANG II (10 −7 M), and this increase was blocked by AT 1 antagonism but not by an AT 2 antagonist. In CRF, colonic protein and mRNA expression variably increased for apical NHE2, NHE3, and ENaC α-, β-, γ-subunits, whereas expression of basolateral NHE1 and Na + -K + -ATPase (α-isoform) remained unaltered. Upregulation of the ENaC subunit mRNA was attenuated somewhat by LOS treatment. Previously, we showed that colonic AT 1 receptor protein is upregulated twofold in CRF, and here we find that AT 1 and AT 2 mRNA and AT 2 protein abundance is unchanged in CRF. We conclude that Na + absorption in CRF rat distal colon is increased due to elevated expression of proteins mediating electroneutral and electrogenic uptake and that it is partially mediated by AT 1 receptors." @default.
- W2022033775 created "2016-06-24" @default.
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- W2022033775 date "2008-08-01" @default.
- W2022033775 modified "2023-09-26" @default.
- W2022033775 title "Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT<sub>1</sub>receptor agonism" @default.
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- W2022033775 doi "https://doi.org/10.1152/ajpgi.00079.2008" @default.
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