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MUCOSAL BIOLOGY

Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT₁ receptor agonism

Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, Florida

Submitted 15 February 2008 ; accepted in final form 2 June 2008

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 AT₁ antagonism but not by an AT₂ antagonist. In CRF, colonic protein and mRNA expression variably increased for apical NHE2, NHE3, and ENaC -, β-, -subunits, whereas expression of basolateral NHE1 and Na⁺-K⁺-ATPase (-isoform) remained unaltered. Upregulation of the ENaC subunit mRNA was attenuated somewhat by LOS treatment. Previously, we showed that colonic AT₁ receptor protein is upregulated twofold in CRF, and here we find that AT₁ and AT₂ mRNA and AT₂ 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 AT₁ receptors.

nephrectomy; angiotensin II; losartan; AT₂ receptor; EIPA

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