17 beta-Estradiol attenuates voltage-dependent Ca2+ currents in A7r5 vascular smooth muscle cell line.
17 beta-Estradiol attenuates voltage-dependent Ca2+ currents in A7r5 vascular smooth muscle cell line.
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DOI：
10.1152/ajpcell.1994.266.4.c975
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发表时间：
1994-04
期刊：
影响因子：
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通讯作者：
F. Zhang;J. Ram;P. Standley;J. Sowers
中科院分区：
文献类型：
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作者：
F. Zhang;J. Ram;P. Standley;J. Sowers
先前的研究表明，17 β-雌二醇（β-E2）对血管平滑肌（VSM）收缩具有直接的急性抑制作用。为了探讨这一现象背后的机制，我们利用全细胞膜片钳技术研究β-E2对培养的VSM细胞（VSMC）电压依赖性Ca ~（2+）通道的影响。在A7 r5培养的VSMC上，用斜坡和脉冲方案表征T和L型Ca 2+电流。在< 100 ms内失活的T型电流可被Ba ~（2+）降低，而伊拉地平对其影响相对较小。L-型电流需要较高的电压才能激活，失活缓慢，被Ba ~（2+）大大增加，并可被5 μ M伊拉地平完全抑制。β-E2（10 μ M）在1-2分钟内显着降低L型Ba 2+电流峰值和T型Ca 2+电流，而α-E2（雌二醇的激素非活性异构体）对这两种类型电流的降低显着较小。溶剂（0.1%乙醇）对任一电流均无显著影响。β-E2对电压依赖性Ca ~（2+）电流的抑制作用可能有助于先前证实的β-E2对VSM收缩的衰减。
Previous studies have shown that 17 beta-estradiol (beta-E2) has a direct acute inhibitory effect on vascular smooth muscle (VSM) contraction. To investigate the mechanisms underlying this phenomenon, we utilized whole cell patch-clamping techniques to study effects of beta-E2 on voltage-dependent Ca2+ channels in cultured VSM cells (VSMC). T- and L-type Ca2+ currents were characterized with ramp and pulse protocols in A7r5 cultured VSMC. T-type current, inactivated in < 100 ms, was reduced by Ba2+ and was comparatively little affected by isradipine. L-type current required higher voltages to activate, inactivated slowly, was greatly increased by Ba2+, and could be completely inhibited by 5 microM isradipine. beta-E2 (10 microM) significantly reduced peak L-type Ba2+ current and T-type Ca2+ current within 1-2 min, whereas alpha E2 (a hormonally inactive isomer of estradiol) caused significantly less reduction in both types of current. Vehicle (0.1% ethanol) had no significant effect on either current. The inhibitory effect of beta-E2 on voltage-dependent Ca2+ currents may contribute to previously demonstrated beta-E2 attenuation of VSM contraction.