Shangold G A, Kongsamut S, Miller R J
Life Sci. 1985 Jun 10;36(23):2209-15. doi: 10.1016/0024-3205(85)90331-5.
We have pharmacologically characterized voltage sensitive calcium channels (VSCCs) in GH3 cells, an anterior pituitary clonal cell line known to secrete prolactin and growth hormone. Raising the medium K+ concentration from 5 to 50 mM caused an immediate increase in net 45Ca2+ uptake which remained apparent over a 15 minute time course. 45Ca2+ uptake was maximally stimulated nearly 10-fold over basal levels. This K+-induced stimulation of Ca2+ uptake was not prevented by 10-5M tetrodotoxin or by replacing sodium with choline in the assay medium. Ca2+ uptake was, however, inhibited by several VSCC antagonists: nitrendipine, D-600, diltiazem and Cd2+. Further, the novel dihydropyridine VSCC agonists, BAY K8644 and CGP 28392, enhanced 50 mM K+-stimulated 45Ca2+ uptake and these effects were blocked by nitrendipine.
我们已对GH3细胞中的电压敏感钙通道(VSCCs)进行了药理学特性分析,GH3细胞是一种已知能分泌催乳素和生长激素的垂体前叶克隆细胞系。将培养基中的钾离子浓度从5 mM提高到50 mM会导致净45Ca2+摄取立即增加,在15分钟的时间进程中这种增加一直很明显。45Ca2+摄取受到最大刺激,比基础水平增加了近10倍。这种钾离子诱导的钙摄取刺激不受10-5M河豚毒素的影响,也不受在测定培养基中用胆碱替代钠的影响。然而,几种VSCC拮抗剂可抑制钙摄取:尼群地平、D-600、地尔硫䓬和Cd2+。此外,新型二氢吡啶VSCC激动剂BAY K8644和CGP 28392增强了50 mM钾离子刺激的45Ca2+摄取,且这些作用被尼群地平阻断。