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 g uinea pig ventricular myocytes. METHODS: Single myocytes were dissociated b y enzymatic dissociation method. The current was recorded with the whole-ce ll configuration of the patch-clamp technique. RESULTS: Dip (0.3 - 30 mu mo l/L) reduced the voltage-dependently activated peak value of ICa-L in a con centration-dependent manner. The characteristics of I-V relationship were n ot greatly altered by Dip, and the maximal activation voltage of ICa-L in t he presence of Dip was not different from that of control. Steady-state act ivation of ICa-L was not affected markedly, and the half activation potenti al (V-0.5) and the slope factor (kappa) in the presence of Dip 3 mu mol/L w ere 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 mu mol/L. The kappa value was (7.1 +/- 0.4) mV in the control and (7.5 /- 0.5) mV in the presence of Dip 3 mu mol/L (n = 7 cells from 3 hearts, P > 0.05). Dip 3 mu mol/L markedly shifted the steady-state inactivation curv e Of ICa-L to the left, and accelerated the voltage-dependent steady-state inactivation of calcium current. V0.5 value was (-19.7 +/- 2.4) mV in the c ontrol and (-31 +/- 6) mV in the presence of Dip 3 mu mol/ L. The kappa val ue was (3.6 +/- 0.3) mV in the control and (1.8 +/- 0.2) mV in the presence of Dip 3 mu mol/L (n = 4 cells from 2 hearts, P < 0.05). Dip 3 <mu>mol/L m arkedly delayed half-recovery time of Ca2+ channel from inactivation from ( 40 +/- 11) to (288 +/- 63) ms (n = 4, P < 0.01). CONCLUSION: Dip mainly act s on the inactivated state of L-type calcium channel, accelerates the inact ivation of calcium channel, and slows the recovery of calcium channel from inactivated state in guinea pig ventricular myocytes, through which the ICa -L is inhibited.