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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Amiodarone Inhibits the Na+-K+ Pump in Rabbit Cardiac Myocytes after Acute and Chronic Treatment

David F. Gray, Anastasia S. Mihailidou, Peter S. Hansen, Kerrie A. Buhagiar, Nerida L. Bewick, Helge H. Rasmussen and David W. Whalley
Journal of Pharmacology and Experimental Therapeutics January 1998, 284 (1) 75-82;
David F. Gray
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Anastasia S. Mihailidou
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Peter S. Hansen
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Kerrie A. Buhagiar
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Nerida L. Bewick
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Helge H. Rasmussen
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David W. Whalley
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Abstract

Amiodarone has been shown to affect cell membrane physicochemical properties, and it may produce a state of cellular hypothyroidism. Because the sarcolemmal Na+-K+ pump is sensitive to changes in cell membrane properties and thyroid status, we examined whether amiodarone affected Na+-K+pump function. We measured Na+-K+ pump current (Ip) using the whole-cell patch-clamp technique in single ventricular myocytes isolated from rabbits. Chronic treatment with oral amiodarone for 4 weeks reduced Ip when myocytes were dialyzed with patch-pipettes containing either 10 mM Na+ or 80 mM Na+. In myocytes from untreated rabbits, acute exposure to amiodarone in vitro reduced Ipwhen patch pipettes contained 10 mM Na+ but had no effect on Ip at 80 mM Na+. Amiodarone had no effect on the voltage dependence of the pump or the affinity of the pump for extracellular K+ either after chronic treatment or during acute exposure. We conclude that chronic amiodarone treatment reduces overall Na+-K+ pump capacity in cardiac ventricular myocytes. In contrast, acute exposure of myocytes to amiodarone reduces the apparent Na+ affinity of the Na+-K+ pump. An amiodarone-induced inhibition of the hyperpolarizing Na+-K+ pump current may contribute to the action potential prolongation observed during treatment with this drug.

Footnotes

  • Send reprint requests to: Dr. David Whalley, Cardiology Department, Royal North Shore Hospital, Pacific Highway, St. Leonards, 2065, Sydney, Australia.

  • ↵1 This study was supported by the National Heart Foundation of Australia (Grant 94S4055) and by the North Shore Heart Research Foundation.

  • ↵2 D.F.G. was the recipient of a National Health and Medical Research Council of Australia Medical Postgraduate Research Scholarship.

  • ↵3 P.S.H. was the recipient of a Postgraduate Medical Research Scholarship from the National Heart Foundation of Australia.

  • Abbreviations:
    Ip
    Na+-K+pump current
    QTc
    corrected QT interval
    T4
    thyroxine
    T3
    triiodothyronine
    HEPES
    N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid
    EGTA
    ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid
    TMA
    tetramethylammonium
    aiNa
    intracellular Na+ activity
    [Na]pip
    pipette Na+ concentration
    [K]o
    extracellular K+ concentration
    K0.5
    concentration for half-maximal pump activation
    Vm
    membrane potential
    Ip-Vm
    pump current-voltage relationship
    • Received April 1, 1997.
    • Accepted September 16, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 284, Issue 1
1 Jan 1998
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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Amiodarone Inhibits the Na+-K+ Pump in Rabbit Cardiac Myocytes after Acute and Chronic Treatment

David F. Gray, Anastasia S. Mihailidou, Peter S. Hansen, Kerrie A. Buhagiar, Nerida L. Bewick, Helge H. Rasmussen and David W. Whalley
Journal of Pharmacology and Experimental Therapeutics January 1, 1998, 284 (1) 75-82;

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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Amiodarone Inhibits the Na+-K+ Pump in Rabbit Cardiac Myocytes after Acute and Chronic Treatment

David F. Gray, Anastasia S. Mihailidou, Peter S. Hansen, Kerrie A. Buhagiar, Nerida L. Bewick, Helge H. Rasmussen and David W. Whalley
Journal of Pharmacology and Experimental Therapeutics January 1, 1998, 284 (1) 75-82;
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