Segmental variability of ENaC subunit expression in rat colon during dietary sodium depletion

E. R. Greig, E. H. Baker, T. Mathialahan, R. P. Boot-Handford, G. I. Sandle

    Research output: Contribution to journalArticlepeer-review

    Abstract

    In rat distal colon, aldosterone has little effect on Na+ channel (ENaC) α-subunit levels but increases the expression of the β- and γ-subunits and stimulates electrogenic Na+ transport. By contrast, the molecular basis of aldosterone's inability to stimulate electrogenic Na+ transport in the proximal colon is unclear. We therefore compared the effects of hyperaldosteronism secondary to 10 days dietary Na+ depletion on ENaC subunit expression in rat proximal and distal colon. Northern analyses revealed appreciable and similar levels of α-subunit mRNA throughout the colon in control and Na+-depleted animals. By contrast, Na+ depletion substantially enhanced β-subunit mRNA expression in the distal colon, but had no effect on the low expression levels of β-subunit mRNA in the proximal colon. Expression of the γ-subunit, evaluated by PCR, was also restricted to the distal colon of Na+-depleted animals. Western analyses demonstrated similar levels of α-subunit protein in the proximal and distal colon of both groups of animals, whereas β-subunit and γ-subunit proteins were detected solely or predominantly in the distal colon of the Na+-depleted animals. Immunocytochemistry confirmed that significant levels of all three subunit proteins only occurred in the apical membrane of surface cells in the distal colon of Na+-depleted animals. Our findings are consistent with previous studies demonstrating that aldosterone stimulates electrogenic Na+ transport in rat distal colon by increasing the expression of β- and γ-subunit mRNA and protein, and thus the amount of functional heteromeric ENaC protein in the apical domain. They also show that aldosterone is incapable of stimulating electrogenic Na+ transport in rat proximal colon (despite the presence of α-subunit mRNA and protein) because of its inability to enhance β- and γ-subunit expression in this segment.
    Original languageEnglish
    Pages (from-to)476-483
    Number of pages7
    JournalPflügers Archiv European Journal of Physiology
    Volume444
    Issue number4
    DOIs
    Publication statusPublished - 2002

    Keywords

    • Aldosterone
    • Amiloride
    • Colon
    • Sodium channel

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