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 (I(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 10 micromol/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 micromol/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 100 micromol/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).
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4728227 | PMC |
| http://dx.doi.org/10.3748/wjg.v9.i1.134 | DOI Listing |
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