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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。
To observe the effect of epinephrine on the C1-current of aortic smooth muscle cells and its relationship with Ca2 + influx, the intracellular free Ca2 + concentration was determined by patch clamp technique and Fura2 fluorescence assay Variety. The results showed that 10 μmol L epinephrine increased the probability of chloride channel opening from 0. 06 ± 0. 0 0 4 2 to 0. 90 90 ± 0. 0 11 in the control group and 1.0 8 ± 0 .2 3ms extended to 6.44 ± 0.57ms. This Cl-current can be inhibited by nifedipine and EGTA. Adrenaline can cause smooth muscle cells within the free Ca2 + concentration from resting at 77 ± 13nmol L rapidly increased peak reached a high level of inflow platform phase, up to 216 ± 27nmol L. Niflumic acid, a Cl-channel blocker, inhibited Cl-current and Ca2 + influx induced by adrenaline in a concentration-dependent manner. The inhibitory rate of 8μmol L niflumic acid to intracellular free Ca2 + was 2 7% ± 8%. The results show that Cl-channel opening plays an important role in the regulation of Ca2 + influx in smooth muscle cells.