Fernando K C, Barritt G J
Department of Medical Biochemistry, School of Medicine, Flinders University of South Australia, Adelaide.
Biochem J. 1994 Oct 15;303 ( Pt 2)(Pt 2):351-6. doi: 10.1042/bj3030351.
The role of heterotrimeric GTP-binding proteins in the process of store-operated Ca2+ inflow in hepatocytes was investigated by testing the ability of pertussis toxin to inhibit thapsigargin- and 2,5-di-tert-butylhydroquinone (DBHQ)-induced bivalent cation inflow. Hepatocytes isolated from rats treated with pertussis toxin for 24 h exhibited markedly inhibited rates of both Ca2+ and Mn2+ inflow when these were stimulated by vasopressin, angiotension II, epidermal growth factor, thapsigargin and DBHQ. Pertussis toxin had little effect on the basal intracellular free Ca2+ concentration ([Ca2+]i), basal rates of Ca2+ and Mn2+ inflow, the abilities of vasopressin, angiotensin II, thapsigargin and DBHQ to induce the release of Ca2+ from intracellular stores, and the maximum value of [Ca2+]i reached following agonist-induced release of Ca2+ from intracellular stores. It is concluded that store-operated Ca2+ inflow in hepatocytes employs a slowly ADP-ribosylated trimeric GTP-binding protein and is the physiological mechanism, or one of the physiological mechanisms, by which vasopressin and angiotensin stimulate plasma membrane Ca2+ inflow in this cell type.
通过检测百日咳毒素抑制毒胡萝卜素和2,5 -二叔丁基对苯二酚（DBHQ）诱导的二价阳离子内流的能力，研究了异源三聚体GTP结合蛋白在肝细胞储存-操作性Ca2+内流过程中的作用。从用百日咳毒素处理24小时的大鼠分离出的肝细胞，当受到血管加压素、血管紧张素II、表皮生长因子、毒胡萝卜素和DBHQ刺激时，Ca2+和Mn2+内流速率均显著受到抑制。百日咳毒素对基础细胞内游离Ca2+浓度（[Ca2+]i）、Ca2+和Mn2+内流基础速率、血管加压素、血管紧张素II、毒胡萝卜素和DBHQ诱导细胞内储存Ca2+释放的能力以及激动剂诱导细胞内储存Ca2+释放后达到的[Ca2+]i最大值几乎没有影响。结论是，肝细胞中储存-操作性Ca2+内流利用一种缓慢ADP核糖基化的三聚体GTP结合蛋白，并且是血管加压素和血管紧张素刺激该细胞类型质膜Ca2+内流的生理机制或生理机制之一。
