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肾上腺素诱导的血管平滑肌细胞C1^-电流及其与Ca^(2+)运动的关系

Adrenaline-Induced Chloride Currents in Vascular Smooth Muscle Cells and its Relationship with Ca^(2+) Movement
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摘要 为观察肾上腺素对主动脉平滑肌细胞C1- 电流的影响及其与Ca2 + 内流的关系 ,采用膜片钳单离子通道(细胞贴附式 )技术和Fura 2荧光法测定细胞内游离Ca2 + 浓度变化。结果发现 ,10 μmol L肾上腺素可引起氯通道开放概率由对照组的 0 .0 6 1± 0 .0 0 4 2增加到 0 .6 90± 0 .0 11;平均开放时间由 1.0 8± 0 .2 3ms延长到 6 .4 4± 0 .5 7ms。此Cl- 电流可被硝苯地平和EGTA抑制。肾上腺素可引起平滑肌细胞内游离Ca2 + 浓度由静息时 77± 13nmol L快速升高达峰值随后维持在高水平的内流平台相 ,达 2 16± 2 7nmol L。Cl- 通道阻断剂尼氟灭酸在一定范围内呈浓度依赖性抑制肾上腺素诱发的Cl- 电流及Ca2 + 内流 ,8μmol L尼氟灭酸对细胞内游离Ca2 + 浓度的抑制率达 2 7%± 8%。结果表明 ,Cl- 通道开放在调节平滑肌细胞Ca2 + 内流中起重要作用。 Aim To investigate the characteristic of chloride currents and Ca 2+ entry induced by adrenaline (Adr) in A10 vascular smooth muscle cells (VSMC). Methods Cell attached patch clamp and Fura 2 fluorescence techniques were used to observe the chloride currents and the changes in [Ca 2+ ]i. Results The open probability (Po)and mean open time(τo) of chloride channels were increased by 10 μmol/L Adr; the Po were increased from 0.061 to 0.69; the τo were increased from 1.08 ms to 6.44 ms. The activatoion of chloride channels were decreased by 10 μmol/L nifedipine and nearly completely inhibited by subsequent addition of 1.5 mmol/L EGTA. Application of Adr activated Ca 2+ influx from the extracellular space. Both of the chloride currents and Ca 2+ influx could be inhibited by the chloride channels blockers niflumic acid (NFA) in a concentration dependent manner. Conclusion The Adr can increase the activation of chloride channels in VSMC and the action is dependent on the extracelluar Ca 2+ influx. The chloride channels play an important role in the regulation of Calcium movement in VSMCs.
出处 《中国动脉硬化杂志》 CAS CSCD 2002年第2期93-96,共4页 Chinese Journal of Arteriosclerosis
基金 国家自然科学基金 (3 9970 849) 广东省自然科学基金团队项目 广东省医学科学技术研究基金 (B2 0 0 0 0 66)
关键词 肾上腺素 平滑 血管 氯通道 膜片钳技术 Adrenaline Muscle, Smooth, Vascular Chloride Channels Patch Clamp Techniques
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