Haloperidol Prolongs Diastolic Phase of Ca^<2+> Transient in Cardiac Myocytes

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Author(s)

Abstract

Haloperidol (HPL), a widely used antipsychotic drug, is known to induce serious ventricular arrhythmias. However, the mechanism underlying their induction is not clear. We therefore examined the effects of HPL on the intracellular Ca<sup>2+</sup> ([Ca<sup>2+</sup>]<sub>i</sub>) transient and on cell motion in cultured cardiac myocytes, as well as the pathways involving the HPL-induced abnormality of Ca<sup>2+</sup> homeostasis. HPL prolonged the diastolic phase of the Ca<sup>2+</sup> transient, with a mid-diastolic re-elevation of [Ca<sup>2+</sup>]<sub>i</sub>. The re-elevation of [Ca<sup>2+</sup>]<sub>i</sub> was shown to be provoked by Ca<sup>2+</sup> release from sarcoplasmic reticulum (SR), which can trigger delayed afterdepolarization, the major arrhythmogenic factor. The re-elevation of [Ca<sup>2+</sup>]<sub>i</sub> coincided with cell re-contraction during diastole. The induction of this abnormality by HPL appears to be independent of the mechanisms of the antipsychotic action.<br>

Journal

  • The Japanese Journal of Physiology

    The Japanese Journal of Physiology 49(6), 479-484, 1999-12-01

    THE PHYSIOLOGICAL SOCIETY OF JAPAN

References:  20

Codes

  • NII Article ID (NAID)
    10008308164
  • NII NACSIS-CAT ID (NCID)
    AA00691224
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    0021521X
  • NDL Article ID
    4979586
  • NDL Source Classification
    ZS8(科学技術--医学--解剖学・生理学・生化学)
  • NDL Call No.
    Z53-D40
  • Data Source
    CJP  NDL  J-STAGE 
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