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Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT1 receptor agonism.
Am J Physiol Gastrointest Liver Physiol. 2008 Aug; 295(2):G348-56.AJ

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 alpha-, beta-, gamma-subunits, whereas expression of basolateral NHE1 and Na(+)-K(+)-ATPase (alpha-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.

Authors+Show Affiliations

Dept. of Pathology, Immunology, and Laboratory Medicine, P.O. Box 100275, 1600 SW Archer Rd., Gainesville, FL 32610, USA. hatchma@ufl.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18535292

Citation

Hatch, Marguerite, and Robert W. Freel. "Increased Colonic Sodium Absorption in Rats With Chronic Renal Failure Is Partially Mediated By AT1 Receptor Agonism." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 295, no. 2, 2008, pp. G348-56.
Hatch M, Freel RW. Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT1 receptor agonism. Am J Physiol Gastrointest Liver Physiol. 2008;295(2):G348-56.
Hatch, M., & Freel, R. W. (2008). Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT1 receptor agonism. American Journal of Physiology. Gastrointestinal and Liver Physiology, 295(2), G348-56. https://doi.org/10.1152/ajpgi.00079.2008
Hatch M, Freel RW. Increased Colonic Sodium Absorption in Rats With Chronic Renal Failure Is Partially Mediated By AT1 Receptor Agonism. Am J Physiol Gastrointest Liver Physiol. 2008;295(2):G348-56. PubMed PMID: 18535292.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT1 receptor agonism. AU - Hatch,Marguerite, AU - Freel,Robert W, Y1 - 2008/06/05/ PY - 2008/6/7/pubmed PY - 2008/9/26/medline PY - 2008/6/7/entrez SP - G348 EP - 56 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am. J. Physiol. Gastrointest. Liver Physiol. VL - 295 IS - 2 N2 - 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 alpha-, beta-, gamma-subunits, whereas expression of basolateral NHE1 and Na(+)-K(+)-ATPase (alpha-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. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/18535292/Increased_colonic_sodium_absorption_in_rats_with_chronic_renal_failure_is_partially_mediated_by_AT1_receptor_agonism_ L2 - http://journals.physiology.org/doi/full/10.1152/ajpgi.00079.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -