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.MET...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.展开更多
AIM: To study the effects of palmatine, a known inhibitoron delayed rectifier potassium current and L-type calciumcurrent (ICa,L) in guinea pig ventricular myocytes, on thepotassium and calcium currents in isolated ra...AIM: To study the effects of palmatine, a known inhibitoron delayed rectifier potassium current and L-type calciumcurrent (ICa,L) in guinea pig ventricular myocytes, on thepotassium and calcium currents in isolated rat hepatocytes.METHODS: Tight-seal wh ole-cell patch-clamp techniqueswere performed to investigate the effects of palmatine onthe delayed outward potassium currents (IK), inward rectifierpotassium current (IK1) and Ca2+ release-activated Ca2+current (ICRAC) in enzymatically isolated rat hepatocytes.RESULTS: Palmatine 0.3-100 μM reduced IK in a concentationdependent manner with EC50of 41.62±10.11 μM and nH,0.48±0.07 (n=8). The effect of the drug was poorly reversibleafter washout. When the bath solution was changed totetraethylammonium (TEA) 8 mM, IK was inhibited.Palmatine 10 μM and 100 μM shifted the I-V curves of IKdownward, and the block of IK was voltage-independent.Palmatine 0.3-100 μM also inhibited ICRAC in a concentration-dependent manner. The fitting parameters were as follows:ECs0=51.19±15.18 μM, and nH=0.46+0.07 (n=8). The peakvalue of ICRAC in the I-V relationship was decreased bypalmatine 10 μM and 100 μM. But the reverse potential ofIcRAcoCcurred at Voltage=0 mV in all cells. Palmatine 0.3-100 μM failed to have any significant effect on either inwardor outward components of IK1 at any membrane potentialexamined.CONCLUSION: The inhibitory effects on IK and ICRAC couldbe one of the mechanisms that palmatine exerts protectiveeffect on hepatocytes.展开更多
文摘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.
文摘AIM: To study the effects of palmatine, a known inhibitoron delayed rectifier potassium current and L-type calciumcurrent (ICa,L) in guinea pig ventricular myocytes, on thepotassium and calcium currents in isolated rat hepatocytes.METHODS: Tight-seal wh ole-cell patch-clamp techniqueswere performed to investigate the effects of palmatine onthe delayed outward potassium currents (IK), inward rectifierpotassium current (IK1) and Ca2+ release-activated Ca2+current (ICRAC) in enzymatically isolated rat hepatocytes.RESULTS: Palmatine 0.3-100 μM reduced IK in a concentationdependent manner with EC50of 41.62±10.11 μM and nH,0.48±0.07 (n=8). The effect of the drug was poorly reversibleafter washout. When the bath solution was changed totetraethylammonium (TEA) 8 mM, IK was inhibited.Palmatine 10 μM and 100 μM shifted the I-V curves of IKdownward, and the block of IK was voltage-independent.Palmatine 0.3-100 μM also inhibited ICRAC in a concentration-dependent manner. The fitting parameters were as follows:ECs0=51.19±15.18 μM, and nH=0.46+0.07 (n=8). The peakvalue of ICRAC in the I-V relationship was decreased bypalmatine 10 μM and 100 μM. But the reverse potential ofIcRAcoCcurred at Voltage=0 mV in all cells. Palmatine 0.3-100 μM failed to have any significant effect on either inwardor outward components of IK1 at any membrane potentialexamined.CONCLUSION: The inhibitory effects on IK and ICRAC couldbe one of the mechanisms that palmatine exerts protectiveeffect on hepatocytes.
