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

应用微电极、膜片钳和等长张力记录技术，研究了雌二醇对兔基底动脉电特性和力学特性的影响。高钾溶液对动脉组织的舒张作用呈浓度依赖性。在无钙溶液中，组胺和咖啡因各自产生阶段性收缩，但雌二醇并没有显着影响其幅度。E2对TEA存在或不存在时的动脉静息膜电位均无明显影响，E2可阻断TEA存在时的动作电位，E2浓度依赖性地抑制电压依赖性Ba电流。在尼卡地平存在下观察到的抑制Ba电流比在尼卡地平的情况下。GTP γ能增强雌二醇对Ba电流的抑制作用。另一方面，在吸管中加入GDP β时，雌二醇不能抑制Ba电流。百日咳毒素（PTX）的吸管完全阻止雌二醇对Ba电流的抑制作用。雌二醇对由膜去极化引起的外向钾电流没有影响，这些结果强烈表明，雌二醇通过抑制电压依赖性钙通道来松弛动脉组织，并且通过PTX敏感的GTP结合蛋白来抑制尼卡地平敏感和抵抗的钙电流。雌二醇在动脉钙通道中的主要靶点似乎是对米卡地平耐药的钙通道，而不是对米卡地平敏感的钙通道。

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.