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。

• 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
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671664/
• 关键词: Estradiol; Vascular smooth muscle; Voltage-clamp; Ca channel; G-protein; voltage-clamp法; エストロゲン; 電位固定法; Ca2+チャンネル; G蛋白

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.

采用微电极、膜片钳和等长张力记录方法研究雌二醇对兔基底动脉电学和力学特性的影响。雌二醇以浓度依赖性方式松弛由过量高钾溶液预收缩的动脉组织。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。无论是否存在 TEA，雌二醇都不会改变动脉的静息膜电位。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。在尼卡地平存在的情况下，雌二醇对 Ba 电流的抑制作用强于不存在尼卡地平的情况。 GTP gamma Sin移液器增强了雌二醇对Ba电流的抑制作用。另一方面，用GDP beta Sin移液器，雌二醇未能抑制Ba电流。移液管中的百日咳毒素（PTX）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 Ca 通道来松弛动脉组织，并且它通过 PTX 敏感的 GTP 结合蛋白抑制尼卡地平敏感和耐药的 Ca 电流。动脉 Ca 通道中雌二醇的主要靶点似乎是米卡地平耐药的 Ca 通道，而不是米卡地平敏感的 Ca 通道。

项目成果

Ogata R et al.,: "Oestradiol-induced relaxation of rabbit basilar artery by inhibition of voltage-dependent Ca channels through GTP-binding protein." British Journal of Pharmacology. (発表予定). (1996)

Ogata R 等人：“雌二醇通过 GTP 结合蛋白抑制电压依赖性 Ca 离子通道诱导兔基底动脉松弛”（英国药理学杂志）（即将出版）。

Ogata R et al.,: "Oestradiol-induced relaxation of rabbit basilar artery by inhibition of voltage-dependent Ca channels through GTP-binding protein" British Journal of Pharmacology. (発足予定). (1996)

Ogata R 等人：“通过 GTP 结合蛋白抑制电压依赖性 Ca 通道，雌二醇诱导兔基底动脉松弛”，《英国药理学杂志》（即将出版）。

Ogata R,Inoue Y,Nakano H,Ito Y and Kitamura K.: "Oestradiol-induced relaxation of rabbit basilar artery by inhibition of volatage-dependent Cachannels through GTP-binding protein." British Journal of Pharmacology. (in press). (1996)

Ogata R、Inoue Y、Nakano H、Ito Y 和 Kitamura K.：“通过 GTP 结合蛋白抑制电压依赖性钙通道，雌二醇诱导兔基底动脉松弛。”