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Cyclosporin A augments angiotensin II-stimulated rise in intracellular free calcium in vascular smooth muscle cells.

机译:环孢菌素A增强血管紧张素II刺激的血管平滑肌细胞内细胞内游离钙的升高。

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摘要

Pretreatment of rat vascular smooth muscle cells with the immunosuppressive drug cyclosporin A caused concentration- and time-dependent increases in both the amplitude and duration of the angiotensin II-induced rise in cytosolic free calcium, as measured with quin 2. Cyclosporin A had no significant effect on basal quin 2 fluorescence. However, cyclosporin A increased the basal 45Ca2+ influx. This stimulation of 45Ca2+ influx was not blocked by nifedipine (10(-6) M). Cyclosporin A also augmented the angiotensin II-stimulated influx and efflux of 45Ca2+. These results demonstrate that cyclosporin A increases the permeability of the plasma membrane for Ca2+ and also augments the angiotensin II-induced increases in cytosolic free calcium.
机译:免疫抑制药物环孢菌素A预处理大鼠血管平滑肌细胞后,浓度和时间依赖性增加了血管紧张素II诱导的胞浆游离钙升高的幅度和持续时间,如喹诺2所测。环孢菌素A无明显意义对基础quin 2荧光的影响。但是,环孢菌素A增加了基础的45Ca2 +内流。硝苯地平(10(-6)M)不会阻止45Ca2 +内流的这种刺激。环孢菌素A还增加了血管紧张素II刺激的45Ca2 +的流入和流出。这些结果证明,环孢菌素A增加了质膜对Ca 2+的渗透性,并且还增加了血管紧张素II诱导的胞质游离钙的增加。

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