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

卵巢类固醇对雌性动物血管平滑肌细胞通道影响的研究。

基本信息

批准号：
06671664
负责人：
INOUE Yoshihito
金额：
$ 1.41万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

项目摘要

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.

雌二醇对兔基底动脉的电气和机械性能的影响通过使用微电极，斑块夹和等距张力记录方法研究。雌二醇以浓度依赖性的方式通过过量的高磷酸溶液预缩的动脉组织。在无CA的溶液中，组胺和咖啡因各自产生质量收缩，但雌二醇并未显着影响其振幅。无论是在存在或不存在茶的情况下，雌二醇都不会改变动脉的静息膜电位。在存在10mm茶的情况下，雌二醇消除了在存在10mm茶的情况下。雌二醇以浓度依赖性方式抑制了依赖电压的BA电流。雌二醇抑制在尼卡迪平存在下观察到的BA电流，而不是在没有尼卡迪胺的情况下。 GTPγsin移液管增强了雌二醇对BA电流的抑制作用。另一方面，用GDP Beta sin驱动器，雌二醇未能抑制BA电流。（PTX）中的百日咳毒素完全阻止了雌二醇对BA电流的抑制作用。雌二醇对膜去极化引起的外向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的Ca通道来松弛动脉组织，并且它抑制了Nicardipine敏感性的CA孔，并且通过PTX敏感的GTP蛋白GTP粘贴蛋白。雌二醇在动脉Ca通道中的主要靶标似乎是耐羊阔定平原的CA通道，而不是对羊甲胺敏感的通道。