摘要
AIM: To study the effects of tetrandrine (Tet) on calciumrelease-activated calcium current (ICRAC), delayed rectifierpotassium current (IK), and inward rectifier potassiumcurrents (IK1) in isolated rat hepatocytes.METHODS: Hepatocytes of rat were isolated by usingperfusion method. Whole cell patch-clamp techniques wereused in our experiment.RESULTS: The peak amplitude.of ICRAC was -508±115 pA(n＝15), its reversal potential of ICRAC was about 0 mV. At thepotential of -100 mV, Tet inhibited the peak amplitude ofICRAC from -521±95 pA to -338±85 pA (P＜0.01 vs control,n＝5), with the inhibitory rate of 35 % at 10 μmol/L andfrom -504±87 pA to -247±82 pA (P＜0.01 vscontrol, n＝5),with the inhibitory rate of 49 % at 100 μmol/L, withoutaffecting its reversal potential. The amplitude of ICRAC wasdependent on extracellular Ca2+ concentration. The peakamplitude of ICRAC was -205±105 pA (n＝3) in tyrode's solutionwith Ca2+ 1.8 mmol/L (P＜0.01 vs the peak amplitude ofICRAC in external solution with Ca2+ 10 mmol/L). Tet at theconcentration of 10 and 100 μmol/L did not markedly changethe peak amplitude of delayed rectifier potassium currentand inward rectifier potassium current (P＞0.05 vs control).CONCLUSION: Tet protects hepatocytes by inhibiting ICRAC,which is not related to I K and IK1.
AIM:To study the effects of tetrandrine(Tet)on calcium release-activated calcium current(I_(CRAC)),delayed rectifier potassium current(I_K),and inward rectifier potassium currents(/_(K1))in isolated rat hepatocytes. METHODS:Hepatocytes of rat were isolated by using perfusion method.Whole cell patch-clamp techniques were used in our experiment. RESULTS:The peak amplitude of I_(CRAC)was-508±115 pA (n=15),its reversal potential of I_(CRAC)was about 0 mV.At the potential of -100 mV,Tet inhibited the peak amplitude of I_(CRAC)from -521±95 pA to -338±85 pA(P<0.01 vs control, n=5),with the inhibitory rate of 35 % at 10μmol/L and from -504±87 pA to -247±82 pA(P<0.01 vs control,n=5), with the inhibitory rate of 49% at 100μmol/L,without affecting its reversal potential.The amplitude of I_(CRAC)was dependent on extracellular Ca^(2+)concentration.The peak amplitude of I_(CRAC)was -205±105 pA(n=3)in tyrode's solution with Ca^(2+)1.8 mmol/L(P<0.01 vs the peak amplitude of I_(CRAC)in external solution with Ca^(2+)10 mmol/L).Tet at the concentration of 10 and 100μmol/L did not markedly change the peak amplitude of delayed rectifier potassium current and inward rectifier potassium current(P>0.05 vs control). CONCLUSION:Tet protects hepatocytes by inhibiting I_(CRAC), which is not related to I_K and I_(K1).
