Volume regulation is defective in renal proximal tubule cells isolated from KCNE1 knockout mice

I. D. Millar, J. A. Hartley, C. Haigh, A. A. Grace, S. J. White, J. D. Kibble, L. Robson

    Research output: Contribution to journalArticlepeer-review

    Abstract

    The membrane protein KCNE1 has been implicated in cell volume regulation. Using a knockout mouse model, this study examined the role of KCNE1 in regulatory volume decrease (RVD) in freshly isolated renal proximal tubule cells. Cell diameter was measured using an optical technique in response to hypotonic shock and stimulation of Na+-alanine cotransport in cells isolated from wild-type and KCNE1 knockout mice. In HEPES buffered solutions 64% of wild-type and 56% of knockout cells demonstrated RVD. In HCO3- buffered solutions 100% of the wild-type cells showed RVD, while in the knockout cells the proportion of cells displaying RVD remained unchanged. RVD in the knockout cells was rescued by valinomycin, a K+ ionophore. In wild-type HCO3- dependent cells the K+ channel inhibitors barium and clofilium inhibited RVD. These data suggest that mouse renal proximal tubule is comprised of two cell populations. One cell population is capable of RVD in the absence of HCO3-, whereas RVD in the other cell population has an absolute requirement for HCO3-. The HCO3- dependent RVD requires the normal expression of KCNE1. © The Physiological Society 2004.
    Original languageEnglish
    Pages (from-to)173-180
    Number of pages7
    JournalExperimental Physiology
    Volume89
    Issue number2
    DOIs
    Publication statusPublished - Mar 2004

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