论文部分内容阅读
缓激肽（BK）可引起PC12细胞的[Ca2＋]i；升高，该作用不通过电压敏感性钙通道，而是由G蛋白转导，通过内钙释放和外钙内流引起的。BK的作用可受到皮质疏（B）的快速抑制。本研究利用无钙／再加钙方法，把BK对内钙释放和外钙内流作用分开来进行研究。结果发现：（1）B可以抑制BK引起的外钙内流，对内钙释放影响不明显；（2）B－BSA（牛血清白蛋自偶联的皮质疏）对BK所引起外钙内流的抑制作用与游离的B作用类似；（3）PKC激活剂（PMA）可以模拟，而PKC的抑制剂G66976可以逆转B的抑制作用；（4）百日咳毒素（PTX）预处理可以阻断B抑制BK引起的外钙内流。结果提示：B可能作用在膜受体上，通过PTX敏感的G蛋白-PKC途径抑制BK引起的外钙内流。
Bradykinin (BK) causes an increase in [Ca2 +] i in PC12 cells, which is not transduced by voltage-sensitive calcium channels but rather by G-protein, resulting from release of endogenous calcium and influx of extracellular calcium. The role of BK can be rapidly inhibited by cortical sparse (B). In this study, calcium-free / calcium-added calcium was used to study the effects of BK on intracellular calcium release and extracellular calcium influx. The results showed that: (1) B can inhibit the influx of extracellular calcium caused by BK and has no obvious effect on the release of intracellular Ca2 +; (2) B-BSA (cortical sparse coupling of bovine serum albumin) Flow inhibition was similar to that of free B; (3) PKC activator (PMA) could be mimicked whereas PKC inhibitor G66976 reversed the inhibitory effect of B; (4) Pertussis toxin (PTX) pretreatment blocked B Inhibit BK-induced extracellular calcium influx. The results suggest that B may act on membrane receptors and inhibit BK-induced extracellular calcium influx through the PTX-sensitive G-protein-PKC pathway.