Maruyama Y
Department of Physiology, Jichi Medical School, Tochigi-Ken, Japan.
Pflugers Arch. 1993 Feb;422(5):476-80. doi: 10.1007/BF00375075.
In single, enzymatically dissociated, rat pancreatic acinar cells, external application of excess divalent cations (Ca2+, Sr2+, Ba2+, Ni2+ and Mg2+ over 50 mM) induced Ca(2+)-dependent current responses monitored with the whole-cell recording technique. Inclusion of either EGTA, heparin or GDP[beta S] in the internal solution or treatment of acinar cells with a phorbol ester abolished the divalent-cation-induced responses. In contrast, internal inositol trisphosphate (InsP3) or GTP[gamma S] potentiated the responses. The results indicate that excess divalent cations activate membrane surface receptors or receptor/effector complexes, thereby inducing InsP3-mediated Ca2+ mobilization. The mechanism may be due to modulation of the receptors by changes in electrical profile through indirect action of divalent cations on membrane surface charges, i.e. neutralization of anionic charges. This proposal was supported by the evidence that the trivalent cation, La3+, and the polyvalent cation, protamine, both at much lower concentrations, could induce Ca(2+)-dependent responses, which were abolished by internal application of heparin, GDP[ beta S] or a high concentration of EGTA or by protein kinase C activation with a phorbol ester.
在单个经酶解离的大鼠胰腺腺泡细胞中，外部施加过量二价阳离子（50 mM以上的Ca2+、Sr2+、Ba2+、Ni2+和Mg2+）会诱导产生Ca(2+)依赖性电流反应，该反应通过全细胞记录技术进行监测。在内液中加入EGTA、肝素或GDP[βS]，或者用佛波酯处理腺泡细胞，均可消除二价阳离子诱导的反应。相反，内部加入肌醇三磷酸（InsP3）或GTP[γS]可增强这些反应。结果表明，过量二价阳离子激活膜表面受体或受体/效应器复合物，从而诱导InsP3介导的Ca2+动员。其机制可能是由于二价阳离子通过对膜表面电荷的间接作用改变电特性来调节受体，即中和阴离子电荷。这一推测得到了以下证据的支持：三价阳离子La3+和多价阳离子鱼精蛋白在低得多的浓度下均可诱导Ca(2+)依赖性反应，而通过在内液中加入肝素、GDP[βS]或高浓度EGTA，或用佛波酯激活蛋白激酶C，这些反应均可被消除。
