Lohr J W, Yohe L A
Department of Medicine (151B), State University of New York at Buffalo 14215.
Brain Res. 1994 Dec 26;667(2):263-8. doi: 10.1016/0006-8993(94)91504-0.
Rat C6 glioma cells undergo regulatory volume decrease (RVD) following hypoosmotic exposure. RVD was inhibited by the K+ channel blockers barium (10 mM) and quinine (1 mM). The mechanism of activation of the volume regulatory process was studied. Volume regulation was not observed following incubation of cells in Ca(2+)-free medium. Fluorescent measurement of intracellular free Ca2+ revealed no change following hypoosmotic exposure. Okadaic acid, an inhibitor of protein phosphatase type 1 and 2A inhibited VRD in C6 glioma cells. These results suggest that hypoosmotic RVD in C6 glioma cells involves a loss of K+ (and anion) from the cell. The activation of K+ loss is dependent on the presence of extracellular calcium (but not an increase in intracellular free calcium); and on protein dephosphorylation, either of a transport protein or another protein in the signalling pathway.
大鼠C6胶质瘤细胞在低渗暴露后会经历调节性容积减小（RVD）。RVD受到钾离子通道阻滞剂钡（10 mM）和奎宁（1 mM）的抑制。对容积调节过程的激活机制进行了研究。在无钙培养基中孵育细胞后未观察到容积调节。细胞内游离钙离子的荧光测量显示，低渗暴露后没有变化。冈田酸是1型和2A型蛋白磷酸酶的抑制剂，它可抑制C6胶质瘤细胞中的VRD。这些结果表明，C6胶质瘤细胞中的低渗RVD涉及细胞内钾离子（和阴离子）的丢失。钾离子丢失的激活依赖于细胞外钙的存在（但不是细胞内游离钙的增加）；以及依赖于信号通路中转运蛋白或其他蛋白的去磷酸化。
