No abstract

Abstract. Effects of haloperidol on L-type Ca V 1.2 channel were studied. Calcium current was measured in whole cell patch-clamp using calcium as a charge carrier. Inhibition by haloperidol was investigated in Ca V 1.2 channel natively expressed in rat cardiac myocytes and recombinant cardiac (Ca V 1.2 a ) and vascular (Ca V 1.2 b ) splice variants of the channel expressed in HEK 293 cells. Haloperidol inhibited L-type calcium current in a concentration-dependent manner with a threshold of 1 nmol/l. 1 μmol/l haloperidol inhibited 20.6 ± 3.6% of calcium current amplitude in cardiomyocytes, 25.4 ± 2.6% of current amplitude through the Ca V 1.2 b channel and 28.0 ± 2.7% of current through the Ca V 1.2 a channel. Inhibition was not accompanied by alteration of current waveform or by shift of current-voltage relation. In a current clamp haloperidol suppressed action potential generation. 1 μmol/l of the drug shortened the action potential duration in part of the cells and suppressed fully action potential in other cells. Moderate inhibition of the L-type calcium channels by haloperidol might cause shortening of action potential. Complete abolishment of action potential must have been mediated by inhibition of another, likely sodium channel.

The gene expression and protein levels of the NCX1 are increased by the strong stress stimuli, e.g. hypoxia, or immobilization stress. The activity of NCX1 is decreased. Based on these results, we assume that the gene expression of NCX is increased as a consequence of suppressed activity of this transport system.

No abstract

Part of the neurotoxic effects of inorganic mercury (Hg 2ϩ ) and methylmercury (MeHg) was attributed to their interaction with voltage-activated calcium channels. Effects of mercury on Ttype calcium channels are controversial. Therefore, we investigated effects of Hg 2ϩ and MeHg on neuronal Ca v 3