Effect Of Valerian Extract On Ionic Channels Of Rabbit Ventricular Myocytes

Objective: To investigate the effects of valerian extract (VE) on action potential duration(APD), sodium current(INa), L-calcium current (Ica-L),transient outward potassium current(Ito), delayed rectifier potrssium current(IK) inward rectifier potassium current(IKl) and adenosine triphosphate-sensitive potassium current (Ikatp) in isolated rabbit ventricular myocytes.Methods: Single rabbit's ventricular myocytes were isolated with enzyme. The whole-cell patch clamp recording technique was used to observe the changes of action potential duration(APD) , sodium current(INa), L-calcium current (ICa-L),transient outward potassium current(Ito), delayed rectifier potassium current(IK), inward rectifier potassium current(IK1) and adenosine triphosphate-sensitive potassium current (Ikatp) under different concentration of VE.Results: (1)30 ug/L VE, 60 u g/L VE could shortened APD50 and APD90 from (352 ±27)ms to (257±24) ms, (168±20)ms, and (416±33)ms to (316±31)ms, (265 ± 23)ms(27.0%, 52.2%; 24.0%,35.6%, n=16, p<0.05) respectively, but had no significant effect on action potential amplitude.(2)VE at 30,60 u g/L decreased peak INa (INamax) from (53.47±5.13)pA/pF to(40.25±4.18)pA/pF and (30.89±2.95)pA/pF (24.7%,41.9%, n=8, p<0.05 and p<0.01), respectively.VE upshifted the INa I-V curves of without changes of their active, peak and reverse potentials; VE at 60 u g/L turned the steady-state inactication curve to right.(3)VE at 30,60 u g/L decreased peak ICa-L (Ica-Lmax) from (6.04±0.59)pA/pF to(3.99±0.31)pA/pF and(2.31±0.24)pA/pF (33.9%,57.1%, n=8, p<0.01), respectively.VE upshifted the I-V curves of Ica-L without changes of their active, peak and reverse potentials; (4)At 60mV, VE at 60 u g/L and 120 u g/L decreased Ito current amplitude from( 4.6±0.42) pA/pF to (2.8±0.23) pA/pF and (1.7±0.14) pA/pF(n=7, p<0.01,respectively);(5)VE did not inhibit Ik, Ik1 with no change on reversal-potential(n=7,p>0.05).(6) VE did not induce Ikatp directly.Conclusion: VE shortened APD in dose-dependent ;VE blocks INa in a concentration dependent manner and probably inhibits Ina in its inactive state ; VE blocks Ica-L manner and probably inhibits Ica-L in its inactive state ; VE inhibited Ito in a concentration dependent ;these could be the important mechanisms of its antiarrhythmic and its cardioprotective effects.