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The heart rate decrease caused by acute FTY720 administration is mediated by the G protein-gated potassium channel I.

Lev Koyrakh1, Maria I Roman, Volker Brinkmann

  • 1Department of Pharmacology, University of Minnesota, Minneapolis, MN 55455, USA.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|February 15, 2005
PubMed
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The immunosuppressant drug FTY720 transiently reduces heart rate by activating the cardiac potassium channel I(KACh). This effect is primarily mediated by the channel, as shown in studies using I(KACh)-deficient mice.

Area of Science:

  • Cardiovascular pharmacology
  • Immunology
  • Molecular signaling

Background:

  • Sphingosine-1-phosphate (S1P) receptors regulate vital cellular processes.
  • The drug FTY720, an S1P analog, is an effective immunosuppressant.
  • FTY720 causes a transient decrease in heart rate (HR).

Purpose of the Study:

  • To investigate the mechanism behind FTY720-induced heart rate reduction.
  • To determine if the cardiac potassium channel I(KACh) is involved in FTY720's effect on HR.

Main Methods:

  • Electrophysiological studies on atrial myocytes from wild-type and I(KACh)-deficient mice.
  • Examined FTY720's active metabolite (FTY720-P) effects on single channel activity and whole-cell currents.
  • Administered FTY720 in vivo to assess HR changes in both mouse models.

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Main Results:

  • FTY720-P activated I(KACh) channels in wild-type myocytes, mimicking acetylcholine.
  • This channel activation was absent in I(KACh)-deficient myocytes.
  • FTY720 caused a dose-dependent HR reduction in wild-type mice, which was significantly blunted in I(KACh)-deficient mice.

Conclusions:

  • Acute FTY720 administration's effect on heart rate is primarily mediated by the activation of the I(KACh) channel.
  • This finding clarifies a key cardiovascular side effect of the immunosuppressant drug FTY720.