环孢素A增强血管平滑肌细胞中血管紧张素II刺激引起的细胞内游离钙升高。
Cyclosporin A augments angiotensin II-stimulated rise in intracellular free calcium in vascular smooth muscle cells.
作者信息
Pfeilschifter J, Rüegg U T
机构信息
Physiologisches Institut der Universität Zürich, Switzerland.
出版信息
Biochem J. 1987 Dec 15;248(3):883-7. doi: 10.1042/bj2480883.
Abstract
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.
摘要
用免疫抑制药物环孢素A预处理大鼠血管平滑肌细胞，会导致血管紧张素II诱导的胞质游离钙升高的幅度和持续时间呈浓度和时间依赖性增加，这是用喹啉2测量得出的结果。环孢素A对基础喹啉2荧光没有显著影响。然而，环孢素A增加了基础45Ca2+内流。硝苯地平（10(-6) M）不能阻断这种对45Ca2+内流的刺激。环孢素A还增强了血管紧张素II刺激的45Ca2+内流和外流。这些结果表明，环孢素A增加了质膜对Ca2+的通透性，并且还增强了血管紧张素II诱导的胞质游离钙升高。
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