Swelling-induced K+ fluxes in vascular smooth muscle cells are mediated by charybdotoxin-sensitive K+ channels

Yana Anfinogenova, Xavier Rodriguez, Ryszard Grygorczyk, Norma Adragna, Peter Lauf, Pavel Hamet, Sergei Orlov

    Research output: Contribution to journalArticle

    16 Citations (Scopus)

    Abstract

    This study examines the relative contributions of K-Cl cotransport and K+ channels to swelling-induced K+ fluxes in vascular smooth muscle cells (VSMC). DIOA known as a potent inhibitor of erythrocyte K-Cl cotransport exerts diverse side-effects on VSMC and can not be used to analyze the role of this carrier in swelling-induced K+ fluxes. Other inhibitors of K-Cl cotransport (furosemide, okadaic acid and calyculin A) did not affect K+ fluxes in VSMC triggered by swelling. Swelling-induced K+ fluxes in VSMC were also not affected by K+ channel blockers such as TEA, glibenclamide and apamin, but were blocked by Ba2+ and charybdotoxin (ChTX), a potent inhibitor of Ca2+-and voltage-gated K+ channels. Swelling-induced K+ influx in VSMC was diminished in Ca2+-free medium and in cells loaded with Ca2+ chelator BAPTA, but was not accompanied by detectable elevation of [Ca2+]i. In contrast to Ca2+-induced hyperpolarization of erythrocytes triggered by activation of intermediate conductance Ca2+-gated K+ channels (IKCa), neither clotrimazole nor calmodulin antagonists (R24571, trifluoroperazine, fluphenazine) affected swelling-induced K+ influx in VSMC. In conclusion, K+ fluxes triggered in swollen VSMC are mediated by Ba2+- and ChTX-sensitive K+ channels. These channels are distinct from IKCa expressed in erythrocytes. Their molecular origin and systems involved in the swelling-induced Ca2+i-independent signal transduction pathway need further investigation.

    Original languageEnglish
    Pages (from-to)295-310
    Number of pages16
    JournalCellular Physiology and Biochemistry
    Volume11
    Issue number6
    DOIs
    Publication statusPublished - 2001

    Fingerprint

    Charybdotoxin
    Vascular Smooth Muscle
    Smooth Muscle Myocytes
    Erythrocytes
    calmidazolium
    Fluphenazine
    Clotrimazole
    Apamin
    Voltage-Gated Potassium Channels
    Trifluoperazine
    Okadaic Acid
    Glyburide
    Furosemide
    Calmodulin
    Chelating Agents
    Signal Transduction

    Keywords

    • Ca
    • Calmodulin
    • Cell swelling
    • K channels
    • K, Cl cotransport
    • Smooth muscle

    ASJC Scopus subject areas

    • Physiology
    • Cell Biology

    Cite this

    Swelling-induced K+ fluxes in vascular smooth muscle cells are mediated by charybdotoxin-sensitive K+ channels. / Anfinogenova, Yana; Rodriguez, Xavier; Grygorczyk, Ryszard; Adragna, Norma; Lauf, Peter; Hamet, Pavel; Orlov, Sergei.

    In: Cellular Physiology and Biochemistry, Vol. 11, No. 6, 2001, p. 295-310.

    Research output: Contribution to journalArticle

    Anfinogenova, Yana ; Rodriguez, Xavier ; Grygorczyk, Ryszard ; Adragna, Norma ; Lauf, Peter ; Hamet, Pavel ; Orlov, Sergei. / Swelling-induced K+ fluxes in vascular smooth muscle cells are mediated by charybdotoxin-sensitive K+ channels. In: Cellular Physiology and Biochemistry. 2001 ; Vol. 11, No. 6. pp. 295-310.
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    AU - Anfinogenova, Yana

    AU - Rodriguez, Xavier

    AU - Grygorczyk, Ryszard

    AU - Adragna, Norma

    AU - Lauf, Peter

    AU - Hamet, Pavel

    AU - Orlov, Sergei

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    AB - This study examines the relative contributions of K-Cl cotransport and K+ channels to swelling-induced K+ fluxes in vascular smooth muscle cells (VSMC). DIOA known as a potent inhibitor of erythrocyte K-Cl cotransport exerts diverse side-effects on VSMC and can not be used to analyze the role of this carrier in swelling-induced K+ fluxes. Other inhibitors of K-Cl cotransport (furosemide, okadaic acid and calyculin A) did not affect K+ fluxes in VSMC triggered by swelling. Swelling-induced K+ fluxes in VSMC were also not affected by K+ channel blockers such as TEA, glibenclamide and apamin, but were blocked by Ba2+ and charybdotoxin (ChTX), a potent inhibitor of Ca2+-and voltage-gated K+ channels. Swelling-induced K+ influx in VSMC was diminished in Ca2+-free medium and in cells loaded with Ca2+ chelator BAPTA, but was not accompanied by detectable elevation of [Ca2+]i. In contrast to Ca2+-induced hyperpolarization of erythrocytes triggered by activation of intermediate conductance Ca2+-gated K+ channels (IKCa), neither clotrimazole nor calmodulin antagonists (R24571, trifluoroperazine, fluphenazine) affected swelling-induced K+ influx in VSMC. In conclusion, K+ fluxes triggered in swollen VSMC are mediated by Ba2+- and ChTX-sensitive K+ channels. These channels are distinct from IKCa expressed in erythrocytes. Their molecular origin and systems involved in the swelling-induced Ca2+i-independent signal transduction pathway need further investigation.

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    KW - Calmodulin

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    KW - K, Cl cotransport

    KW - Smooth muscle

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