THE CALCIUM-CHANNEL CURRENT OF PREGNANT RAT SINGLE MYOMETRIAL CELLS IN SHORT-TERM PRIMARY CULTURE
THE CALCIUM-CHANNEL CURRENT OF PREGNANT RAT SINGLE MYOMETRIAL CELLS IN SHORT-TERM PRIMARY CULTURE
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DOI：
10.1113/jphysiol.1987.sp016779
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发表时间：
1987-11-01
影响因子：
5.5
通讯作者：
MIRONNEAU, J
中科院分区：
文献类型：
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作者：
AMEDEE, T;MIRONNEAU, C;MIRONNEAU, J
1.用单电极电压钳或电流钳分析了短期原代培养的孕鼠单个子宫肌细胞的被动和主动电特性。2.在四乙基氯化铵和4-氨基吡啶（各10 mM）的存在下，并与Cs+溶液（4 M）中的微电极记录动作电位和膜电流。3.研究了电压依赖性、Ca ~（2+）拮抗剂的作用以及Sr ~（2+）或Ba ~（2+）取代的影响。在10 mM-Ca 2+溶液中，峰值Ca 2+电流密度在15-20 μ A/cm 2的范围内。4.根据钙通道电流的反向电位测量和经表面电荷校正后的内向电流比较，钙通道对二价阳离子的相对选择性顺序为Ca ~（2+）> Sr ~（2+）= Ba ~（2+）。5.当外源Ca ~（2+）被Sr ~（2+）或Ba ~（2+）替代时，Ca ~（2+）通道电流衰减减慢。衰减反映了失活的Ca 2+通道电导，作为评估的内向尾电流的幅度逐渐变长的去极化和稳定值的逆转电位时，Ca 2+通道电流增加在调节脉冲。6.电压依赖性失活说明了外向钙通道电流由于K+和/或Cs+外流与外部Ba 2+或在没有任何永久性二价阳离子的失活。7. 双脉冲法测定细胞内Ca ~（2+）浓度与失活的关系。产生最大Ca 2+电流的条件脉冲诱导最大失活：随着去极化的增强，失活减少，但在预期的Ca 2+逆转电位下不能完全阻止。在预脉冲期间增加进入细胞的Ca 2+的量降低了测试Ca 2+电流的幅度和动力学。在Ba 2+作为电荷载体的情况下未观察到该结果。8. Ca 2+通道电流失活最好用双指数函数拟合。在Ba ~（2+）溶液中的快失活时间常数比在Ca ~（2+）溶液中大，但两个时间常数随膜电位的变化不大。失活的慢时间常数是陡峭的电压依赖性。9.在Ca 2+和Ba 2+溶液中，失活的恢复被描述为双指数过程。当Ba ~（2+）离子为电荷载体时，只有较慢的恢复时间常数降低。10.我们的结论是，孤立的子宫肌层Ca 2+通道的失活是依赖于内部Ca 2+浓度和膜电位。
1. The passive and active electrical properties of pregnant rat single myometrial cells in short-term primary culture were analysed using a single-electrode voltage or current clamp. 2. Action potentials and membrane currents were recorded in the presence of tetraethylammonium chloride and 4-aminopyridine (10 mM each) and with Cs+ solution (4 M) in the microelectrode. 3. The voltage dependence, the action of Ca2+ antagonists and the effects of Sr2+ or Ba2+ substitution were studied. The peak Ca2+ current density was in the range 15-20 .mu.A/cm2 in 10 mM-Ca2+ solution. 4. According to both measurement of the reversal potential of Ca2+ channel currents and comparison of the inward currents after correction for changing surface charge, the relative selectivity sequence of the Ca2+ channel for divalent cations was Ca2+ > Sr2+ = Ba2+. 5. The decay of Ca2+ channel current during a maintained depolarization was slowed when external Ca2+ was replaced by Sr2+ or Ba2+. The decay reflected an inactivation of Ca2+ channel conductance, as assessed by the decreased amplitude of inward tail currents following progressively longer depolarizations and the stable value of the reversal potential when Ca2+ channel current was increased during conditioning pulses. 6. Voltage-dependent inactivation was illustrated by inactivation of outward Ca2+ channel current due to K+ and/or Cs+ efflux with external Ba2+ or in the absence of any permanent divalent cation. 7. The relationship between inactivation and the intracellular Ca2+ concentration was assessed by a double-pulse method. Conditioning pulses that produced maximal Ca2+ current induced maximal inactivation: with stronger depolarizations inactivation decreased but was not completely prevented at the expected Ca2+ reversal potential. Increasing the amount of Ca2+ entering the cell during the pre-pulse reduced both amplitude and the kinetics of test Ca2+ currents. The results were not observed with Ba2+ as the charge carrier. 8. Ca2+ channel current inactivation was best fitted by a two-exponential function. The fast time constant of inactivation was larger in Ba2+ solution than in Ca2+ solution but both time constants showed little variation with membrane potential. The slow time constants of inactivation were steeply voltage dependent. 9. Recovery from inactivation was described as a two-exponential process in both Ca2+ and Ba2+ solutions. Only the slower time constant of recovery was decreased when Ba2+ ions were the charge carrier. 10. We conclude that inactivation of isolated myometrial Ca2+ channels is dependent on both internal Ca2+ concentration and membrane potential.