Shimahara T, Icard-Liepkalins C, Ohmori H, Shigemoto T
Laboratoire de Neurobiologie Cellulaire et Moléculaire C.N.R.S., Gif-sur-Yvette, France.
Brain Res. 1990 Aug 6;524(2):219-24. doi: 10.1016/0006-8993(90)90694-7.
Bradykinin triggered intracellular Ca mobilizations and ionic conductance changes were studied in the neuroblastoma x glioma hybrid cell line NG108-15 using Ca-sensitive fluorescent indicator fura-2 under patch pipette whole cell voltage clamp condition. The time course of outward current induced by bradykinin was closely related to the time-course of [Ca2+]i change. Following application of bradykinin, [Ca2+]i increased transiently and then decreased below the basal level before bradykinin application. The inward currents activated by step-depolarization were suppressed after bradykinin application, but the time-course of the suppression did not go in parallel with the [Ca2+]i changes: the suppression started before the [Ca2+]i change emerged and outlasted the phase of [Ca2+]i increase. Both transient type and long-lasting type Ca current were suppressed by bradykinin. [Ca2+]i increase induced by high potassium depolarization was suppressed by bradykinin. Pertussis toxin did not affect the Ca transient nor the suppression of Ca channel induced by bradykinin. Our results suggest that the modifications of ionic channels by bradykinin could be through the other mechanisms than the well established activation of the G-protein leading to the IP3 mechanisms and that the bradykinin receptor might couple with the pertussis toxin-insensitive G protein which regulates the calcium channels.
在膜片吸管全细胞电压钳制条件下，使用钙敏荧光指示剂fura-2，研究了缓激肽在神经母细胞瘤x胶质瘤杂交细胞系NG108-15中引发的细胞内钙动员和离子电导变化。缓激肽诱导的外向电流的时间进程与[Ca2+]i变化的时间进程密切相关。施加缓激肽后，[Ca2+]i短暂升高，然后在施加缓激肽之前降至基础水平以下。缓激肽施加后，阶跃去极化激活的内向电流受到抑制，但抑制的时间进程与[Ca2+]i变化不平行：抑制在[Ca2+]i变化出现之前开始，且在[Ca2+]i升高阶段之后持续存在。缓激肽抑制了瞬态型和长效型钙电流。缓激肽抑制了高钾去极化诱导的[Ca2+]i升高。百日咳毒素不影响钙瞬变，也不影响缓激肽诱导的钙通道抑制。我们的结果表明，缓激肽对离子通道的修饰可能通过不同于已确立的激活G蛋白导致IP3机制的其他机制，并且缓激肽受体可能与调节钙通道的百日咳毒素不敏感G蛋白偶联。
