Effect of dipfluzine on L-type calcium current in guinea pig ventricular myocytes

AIM: To study the effect of dipfluzine (Dip) on L-type calcium current in guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. The current was recorded with the whole-cell configuration of the patch-clamp technique. RESULTS: Dip (0.3 - 30 μmol/L) reduced the voltage-dependently activated peak value of I_Ca-L in a concentration-dependent manner. The characteristics of I-V relationship were not greatly altered by Dip, and the maximal activation voltage of I_Ca-L in the presence of Dip was not different from that of control. Steady-state activation of I_Ca-L was not affected markedly, and the half activation potential (V_0.5) and the slope factor (κ) in the presence of Dip 3 μmol/L were not markedly different from those of the control. V_0.5 value was ( -12.8 ± 1.7) mV in the control and ( -13.2 ± 2.4) mV in the presence of Dip 3 μmol/L. The κ value was (7.1 ± 0.4) mV in the control and (7.5 ± 0.5) mV in the presence of Dip 3 μmol/L (n = 7 cells from 3 hearts, P > 0.05). Dip 3 μmol/L markedly shifted the steady-state inactivation curve of I_Ca-L to the left, and accelerated the voltage-dependent steady-state inactivation of calcium current. V_0.5 value was ( -19.7 ± 2.4) mV in the control and ( -31 ± 6) mV in the presence of Dip 3 μmol/L. The κ value was (3.6 ± 0.3) mV in the control and (1.8 ± 0.2) mV in the presence of Dip 3 μmol/L (n = 4 cells from 2 hearts, P < 0.05). Dip 3 μmol/L markedly delayed half-recovery time of Ca²⁺ channel from inactivation from (40 ± 11) to (288 ± 63) ms (n = 4, P < 0.01). CONCLUSION: Dip mainly acts on the inactivated state of L-type calcium channel, accelerates the inactivation of calcium channel, and slows the recovery of calcium channel from inactivated state in guinea pig ventricular myocytes, through which the I_Ca-L is inhibited.