G Y Cui, J M Li, H Cui, L Y Hao, D J Liu, K Y Zhang
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引用次数: 0
摘要
目的:研究钙通道阻滞剂对大鼠肝细胞钙释放激活钙电流(ICRAC)的影响。方法:采用全细胞膜片钳技术。结果:ICRAC的峰值为-0.41 nA +/- 0.09 nA (n = 15)，其逆转电位约为0 mV。维拉帕米(Ver)、地尔硫卓(Dil)和硝苯地平(Nif)显著降低ICRAC，但不影响其逆转潜能。ver5 mumol的抑制率。L-1为40% +/- 12% (n = 3)， Ver 50 μ mol。L-1使ICRAC的峰幅由-0.49 nA +/- 0.12 nA降低至-0.20 nA +/- 0.09 nA (P < 0.01, n = 5)，抑制率为57% +/- 15%。50毫升。L-1和Nif使ICRAC从-0.43 nA +/- 0.10 nA降至-0.29 nA +/- 0.07 nA (P < 0.01, n = 5)，从-0.32 nA +/- 0.08 nA降至-0.27 nA +/- 0.08 nA (P < 0.01, n = 5)，抑制率分别为31% +/- 11%、19% +/- 7%。ICRAC的振幅依赖于细胞外Ca2+浓度。在Ca2+ 1.8 mmol的Tyrode溶液中，ICRAC的峰值为-0.21 nA +/- 0.08 nA (n = 3)。与Ca2+ 10 mmol.L-1外溶液中ICRAC的峰值幅度相比，P < 0.01)。结论:3种钙拮抗剂能有效抑制ICRAC，并通过抑制ICRAC来保护肝细胞钙超载。
Effects of calcium channel blockers on calcium release-activated calcium currents in rat hepatocytes.
Aim: To study the influences of calcium channel blockers on calcium release-activated calcium currents (ICRAC) in rat hepatocytes.
Methods: Whole-cell patch-clamp technique was used.
Results: The peak amplitude of ICRAC was -0.41 nA +/- 0.09 nA (n = 15), its reversal potential was about 0 mV. Verapamil (Ver), diltiazem (Dil), and nifedipine (Nif) decreased ICRAC strikingly, without affecting its reversal potential. The inhibitory rate of Ver 5 mumol.L-1 was 40% +/- 12% (n = 3), Ver 50 mumol.L-1 reduced the peak amplitude of ICRAC from -0.49 nA +/- 0.12 nA to -0.20 nA +/- 0.09 nA (P < 0.01 vs control, n = 5). The inhibitory rate was 57% +/- 15%. Dil 50 mumol.L-1 and Nif reduced ICRAC from -0.43 nA +/- 0.10 nA to -0.29 nA +/- 0.07 nA (P < 0.01 vs control, n = 5), from -0.32 nA +/- 0.08 nA to -0.27 nA +/- 0.08 nA (P < 0.01 vs control, n = 5). The inhibitory rate was 31% +/- 11%, 19% +/- 7%, respectively. The amplitude of ICRAC was dependent on extracellular Ca2+ concentration. The peak amplitude of ICRAC was -0.21 nA +/- 0.08 nA (n = 3) in Tyrode's solution with Ca2+ 1.8 mmol.L-1 (P < 0.01 vs the peak amplitude of ICRAC in external solution with Ca2+ 10 mmol.L-1).
Conclusion: The three calcium antagonists inhibited ICRAC effectively and protected hepatocytes from calcium overload via the inhibition of ICRAC.
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