RESEARCH FOR THE EFFECTS OF OVARIAN STEROIDS ON THE CHANNELS OF VASCULAR SMOOTH MUSCLE CELLS OBTAINED FROM FEMALE ANIMAL.

采用微电极法、膜片钳法和等长张力记录法研究雌二醇对兔基底动脉电学和力学性能的影响。雌二醇对过量高钾溶液预收缩的动脉组织有浓度依赖性的松弛作用。在不含ca的溶液中，组胺和咖啡因均产生相性收缩，但雌二醇对其幅度没有显著影响。雌二醇不改变动脉静息膜电位，无论存在或不存在TEA。在10mM TEA存在下观察到的动作电位被雌二醇消除。雌二醇以浓度依赖性方式抑制电压依赖性Ba电流。雌二醇在有尼卡地平时比无尼卡地平时更能抑制Ba电流。GTP - γ - Sin移液管增强雌二醇对Ba电流的抑制作用。另一方面，与GDP β Sin移液管，雌二醇未能抑制Ba电流。百日咳毒素（PTX）移液管完全阻止雌二醇对Ba电流的抑制作用。雌二醇对膜去极化引起的向外K电流没有影响。这些结果强烈表明，雌二醇通过抑制电压依赖性钙通道使动脉组织松弛，并通过ptx敏感的gtp结合蛋白抑制nicardipine敏感和抗性钙电流。雌二醇在动脉钙通道中的主要靶点似乎是耐米地平钙通道，而不是米地平敏感钙通道。

Effects of estradiol on the electrical and mechanical properties of the rabbit basilar artery were investigated by use of microelectrode, patch-clamp and isometric tension recording methods. Estradiol relaxd arterial tissue pre-contracted by excess high-potassium solution in a concentration dependent manner. In Ca-free solution, histamine and caffeine each produced a phasic contraction, but estradiol did not significantly affect their amplitude. Estradiol did not change the resting membrane potential of the artery whether in the presence or absence of TEA.Action potentials observed in the presence of 10mM TEA were abolished by estradiol.Estradiol inhibited the voltage-dependent Ba current in a concentration-dependent manner. Estradiol inhibited Ba current observed in the presence of nicardipine more than that in the absence of nicardipine. GTP gamma Sin the pipette enhanced the inhibitory actions of estradiol on the Ba current. On the other hand, with GDP beta Sin the pipette, estradiol failed to inhibit the Ba current. Pertussis toxin in (PTX) the pipette totally prevented the inhibitory action of estradiol on the Ba current. Estradiol had no effect on the outward K currents evoked by a membrane depolarization.These results strongly suggest that estradiol relaxs arterial tissue by inhibition of voltage-dependent Ca channels and that it inhibits both nicardipine-sensitive and-resistant Ca currents via a PTX-sensitive GTP-binding protein. The main target of estradiol among the arterial Ca channels seems to be the micardipine-resistant Ca channel, rather than the micardipine-sensitive one.