Published online Jan 15, 2003. doi: 10.3748/wjg.v9.i1.134
Revised: July 10, 2002
Accepted: July 25, 2002
Published online: January 15, 2003
AIM: To study the effects of tetrandrine (Tet) on calcium release-activated calcium current (ICRAC), delayed rectifier potassium current (IK), and inward rectifier potassium currents (IK1) 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 ICRAC was -508 ± 115 pA (n = 15), its reversal potential of ICRAC was about 0 mV. At the potential of -100 mV, Tet inhibited the peak amplitude of ICRAC 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 and from -504 ± 87 pA to -247 ± 82 pA (P < 0.01 vs control, n = 5), with the inhibitory rate of 49% at 100 µmol/L, without affecting its reversal potential. The amplitude of ICRAC was dependent on extracellular Ca2+ concentration. The peak amplitude of ICRAC was -205 ± 105 pA (n = 3) in tyrode’s solution with Ca2+ 1.8 mmol/L (P < 0.01 vs the peak amplitude of ICRAC in external solution with Ca2+ 10 mmol/L). Tet at the concentration of 10 and 100 µmol/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 ICRAC, which is not related to IK and IK1.