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. 2014 Nov 10;37(11):804–811. doi: 10.14348/molcells.2014.0167

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Fig. 3. — Effect of ω-CgTx on I_Ca and PAR-2 agonist-induced I_Ca inhibition. (A) Left, a representative trace showing the effect of consecutive application of ω-CgTx (1 μM) and nifedipine (1 μM) on I_Ca. Right, time course of the effects induced by consecutive application of ω-CgTx (1 μM) and nifedipine (1 μM) on I_Ca. Trace 1, 2, and 3 in the left panel represent the traces recorded at the corresponding time indicated in the right panel, respectively. (B) Contribution of N-type (ω-CgTx-sensitive) and L-type (nifedipine-sensitive) currents to the total I_Ca. (C) Left, a representative trace of the effects induced by consecutive application of ω-CgTx (1 μM) and trypsin (30 nM) on I_Ca. Right, time course of effects induced by consecutive application of ω-CgTx (1 μM) and trypsin (30 nM) on I_Ca.Trace 1, 2, and 3 in the left panel represent the traces recorded at the corresponding time indicated in the right panel, respectively. (D) Summary of I_Ca inhibition by trypsin in the absence and presence of ω-CgTx. (E) Left, a representative trace of the effects induced by consecutive application of ω-CgTx (1 μM) and SL-NH₂ (100 μM) on I_Ca. Right, time course of effects induced by consecutive application of ω-CgTx (1 μM) and SL-NH₂ (100 μM) on I_Ca. Trace 1, 2, and 3 in the left panel represent the traces recorded at the corresponding time indicated in the right panel, respectively. (F) Summary of I_Ca inhibition by SL-NH₂ in the absence and presence of ω-CgTx.