Effects of taurine-magnesium coordination compound on ionic channels in rat ventricular myocytes of arrhythmia induced by ouabain.

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  • Author(s): Zhao L;Zhao L; Lou J; Wu H; Yin Y; Kang Y
  • Source:
    Biological trace element research [Biol Trace Elem Res] 2012 Jun; Vol. 147 (1-3), pp. 275-84. Date of Electronic Publication: 2012 Feb 05.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Humana Press Country of Publication: United States NLM ID: 7911509 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-0720 (Electronic) Linking ISSN: 01634984 NLM ISO Abbreviation: Biol Trace Elem Res Subsets: MEDLINE
    • Publication Information:
      Original Publication: [London, Clifton, N. J.] Humana Press.
    • Subject Terms:
      Ion Channels/*physiology ; Magnesium/*pharmacology ; Myocytes, Cardiac/*drug effects ; Organometallic Compounds/*pharmacology ; Ouabain/*pharmacology ; Taurine/*pharmacology; Amiodarone/pharmacology ; Animals ; Anti-Arrhythmia Agents/pharmacology ; Calcium Channels, L-Type/physiology ; Cardiotonic Agents/pharmacology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Female ; Heart Ventricles/cytology ; Magnesium/chemistry ; Male ; Membrane Potentials/drug effects ; Myocytes, Cardiac/physiology ; Organometallic Compounds/chemistry ; Patch-Clamp Techniques ; Potassium Channels/physiology ; Rats ; Rats, Wistar ; Taurine/chemistry
    • Abstract:
      Taurine-magnesium coordination compound (TMCC) has anti-arrhythmic effects. The aim of the present study was to explore the targets of the anti-arrhythmic effect of TMCC and the electrophysiological effects of TMCC on ouabain-induced arrhythmias in rat ventricular myocytes. Sodium current (I(Na)), L-type calcium current (I(ca, L)), and transient outward potassium current (I(to)) were measured and analyzed using whole-cell patch-clamp recording technique in normal rat cardiac myocytes and rat ventricular myocytes of arrhythmia induced by ouabain. In isolated ventricular myocytes, I(Na) and I(to) were blocked by TMCC (100, 200, 400 μM) in a concentration-dependent manner, and the effects of TMCC (400 μM) were equal to that of amiodarone. However, I (ca, L) was moderately increased by TMCC (400 μM) while significantly decreased by amiodarone. Ouabain (5 μM) significantly decreased sodium, L-type calcium, and transient outward potassium currents. TMCC (100 μM) relieved abnormal sodium currents induced by ouabain through facilitation of steady-state inactivation. TMCC (200 and 400 μM) relieved abnormal L-type calcium currents induced by ouabain through facilitation of steady-state activation and retardation of steady-state inactivation. TMCC failed to further inhibit abnormal transient outward potassium currents induced by ouabain. However, amiodarone inhibited the decreasing sodium, L-type calcium, and transient outward potassium currents further. These data suggest that I(Na), I(ca, L), and I(to) may be the targets of the antiarrhythmic effect of TMCC, which can antagonize ouabain-induced changes of ionic currents in rat ventricular myocytes.
    • Accession Number:
      0 (Anti-Arrhythmia Agents)
      0 (Calcium Channels, L-Type)
      0 (Cardiotonic Agents)
      0 (Ion Channels)
      0 (Organometallic Compounds)
      0 (Potassium Channels)
      1EQV5MLY3D (Taurine)
      5ACL011P69 (Ouabain)
      I38ZP9992A (Magnesium)
      N3RQ532IUT (Amiodarone)
    • Publication Date:
      Date Created: 20120208 Date Completed: 20121003 Latest Revision: 20131121
    • Publication Date:
      20231215
    • Accession Number:
      10.1007/s12011-011-9317-1
    • Accession Number:
      22311082