Oiki S, Ueda S, Okada Y
Biochem Biophys Res Commun. 1985 Oct 15;132(1):290-8. doi: 10.1016/0006-291x(85)91021-6.
By means of Ca2+- and K+-selective microelectrodes, the changes in intracellular free Ca2+ and K+ were measured during the hyperpolarizing responses induced by ATP, complement and beta-lipoprotein in mouse fibroblastic L cells. The cytoplasmic Ca2+ concentration [( Ca]i) was about 0.4 microM in the resting state. The hyperpolarizing responses always coincided with a phasic increase in [Ca]i. ATP or beta-lipoprotein induced about a 2-fold rise in [Ca]i, and complement did up to 3-fold. Both the hyperpolarizing responses and [Ca]i increases were prevented by removal of external Ca2+ or by application of a Ca-channel blocker, nifedipine. Quinine, a Ca-activated K-channel inhibitor, suppressed the hyperpolarizing responses but not the [Ca]i increases. During the hyperpolarizing response, the intracellular free K+ concentration gradually decreased from about 120 to 110 mM. Thus, it is concluded that ATP, complement and beta-lipoprotein caused a transient elevation of cytoplasmic free Ca2+ due to Ca2+ influxes, thereby inducing electrical membrane responses through activation of Ca-dependent K-channels in the fibroblasts.
通过钙离子和钾离子选择性微电极，在小鼠成纤维细胞L中，测量了ATP、补体和β-脂蛋白诱导的超极化反应过程中细胞内游离钙离子和钾离子的变化。静息状态下细胞质钙离子浓度[(Ca)i]约为0.4微摩尔。超极化反应总是与[(Ca)i]的阶段性增加同时出现。ATP或β-脂蛋白诱导[(Ca)i]升高约2倍，补体则高达3倍。去除细胞外钙离子或应用钙通道阻滞剂硝苯地平可阻止超极化反应和[(Ca)i]的增加。钙激活钾通道抑制剂奎宁可抑制超极化反应，但不抑制[(Ca)i]的增加。在超极化反应过程中，细胞内游离钾离子浓度从约120毫摩尔逐渐降至110毫摩尔。因此，得出结论：ATP、补体和β-脂蛋白由于钙离子内流导致细胞质游离钙离子短暂升高，从而通过激活成纤维细胞中的钙依赖性钾通道诱导电膜反应。
