Halenda S P, Rehm A G
Department of Pharmacology, University of Missouri-Columbia 65212.
Biochem J. 1987 Dec 1;248(2):471-5. doi: 10.1042/bj2480471.
Human platelets were depleted of intracellular Ca2+ and then made selectively permeable to external Ca2+ by addition of the ionophore ionomycin. In this cell system a rapid release of arachidonic acid was seen in direct response to added Ca2+ at concentrations corresponding to cytosolic Ca2+ levels measured in thrombin-stimulated platelets. Thrombin and other activators of Ca2+/phospholipid-dependent protein kinase (C-kinase) potentiated the Ca2+-stimulated arachidonic acid release while exerting little or no effect in the absence of added Ca2+. Agents which increase (R59022) or decrease (isoquinolinesulphonylmethylpiperazine) the activation of C-kinase correspondingly enhanced or inhibited, respectively, the potentiation of arachidonic acid release caused by thrombin. These results support the hypothesis that arachidonic acid release in human platelets is regulated by a co-operative action between intracellular Ca2+ and C-kinase.
将人血小板内的细胞内钙离子耗尽,然后通过添加离子载体离子霉素使其对细胞外钙离子具有选择性通透性。在这个细胞系统中,在添加与凝血酶刺激血小板时测量的胞质钙离子水平相对应浓度的钙离子后,可直接观察到花生四烯酸的快速释放。凝血酶和其他钙离子/磷脂依赖性蛋白激酶(C激酶)激活剂增强了钙离子刺激的花生四烯酸释放,而在未添加钙离子时几乎没有影响。增加(R59022)或降低(异喹啉磺酰甲基哌嗪)C激酶活性的试剂分别相应地增强或抑制了凝血酶引起的花生四烯酸释放增强作用。这些结果支持了这样一种假说,即人血小板中花生四烯酸的释放是由细胞内钙离子和C激酶的协同作用调节的。