Effect of haloperidol on voltage dependent cardiac ion channels

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Authors

TARABOVÁ Bohuslava NOVÁKOVÁ Marie BÉBAROVÁ Markéta PÁSEK Michal MATEJOVIČ Peter LACINOVÁ Lubica

Year of publication 2004
Type Article in Proceedings
Conference Membrane Channels, Transporters and Receptors
MU Faculty or unit

Faculty of Medicine

Citation
Field Physiology
Keywords haloperidol; patch clamp; rat cardiomyocytes; HEK 293 cells
Description Haloperidol is a neuroleptic agent effective in treatment of various psychiatric diseases. Cardiac arrhythmias have been associated with this therapy. We have investigated effects of haloperidol on cardiac sodium, potassium and calcium channels using whole cell patch-clamp method. 10 microM concentration of haloperidol was tested. In cardiomyocytes isolated from adult rat ventricles, haloperidol inhibited 95% of sodium current (INa) activated by 40 ms voltage pulses from -75 mV to -20 mV. The block of the transient outward potassium current (Ito) and current at the end of the pulse (IK,end) were measured by 300 ms voltage pulses from -75 mV to +40 mV. Haloperidol caused 80% block of Ito and 37% block of IK,end. In all cases the block was reversible. Further, we have investigated CaV1.2 L-type calcium channel transiently expressed in HEK 293 cells. Haloperidol inhibited approximately 58% of inward current amplitude measured in peak of IV relation. The inhibition was reversible and voltage dependent. Increasing amplitude of depolarizing pulses increased strongly extent of current inhibition.
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