Lopez-Rivas A, Rozengurt E
Am J Physiol. 1984 Sep;247(3 Pt 1):C156-62. doi: 10.1152/ajpcell.1984.247.3.C156.
Addition of the neurohypophysial nonapeptide [Arg8]vasopressin to 45Ca2+-loaded quiescent cultures of Swiss 3T3 cells or diploid mouse embryo fibroblasts causes a rapid increase (within seconds) in the rate of 45Ca2+ efflux from the cells. This reflects the release of 45Ca2+ from an intracellular store that is partly or entirely derived from mitochondria and leads to a marked decrease (52%) in the intracellular 45Ca2+ content of the cultures under equilibrium 45Ca2+ conditions. The effect is dose dependent, specific, and blocked by a vasopressor antagonist. Prolonged pretreatment with vasopressin that renders the cells unresponsive to the mitogenic effects of the hormone also blocks the Ca2+ response. The results suggest that Ca2+ fluxes may be involved in the mechanism of mitogenic action of vasopressin in Swiss 3T3 cells.
向加载了45Ca2+的静止状态的瑞士3T3细胞或二倍体小鼠胚胎成纤维细胞培养物中添加神经垂体九肽[Arg8]血管加压素,会导致细胞中45Ca2+外流速率迅速增加(数秒内)。这反映了45Ca2+从部分或完全源自线粒体的细胞内储存库中释放出来,并导致在平衡45Ca2+条件下培养物的细胞内45Ca2+含量显著降低(52%)。该效应具有剂量依赖性、特异性,并被血管升压拮抗剂阻断。用血管加压素进行长时间预处理使细胞对该激素的促有丝分裂作用无反应,也会阻断Ca2+反应。结果表明,Ca2+通量可能参与血管加压素对瑞士3T3细胞的促有丝分裂作用机制。