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小鼠垂体瘤细胞中的多种钙通道类型。

Multiple classes of calcium channels in mouse pituitary tumor cells.

作者信息

Richardson U I

出版信息

Life Sci. 1986 Jan 6;38(1):41-50. doi: 10.1016/0024-3205(86)90273-0.

Abstract

Synthetic corticotropin-releasing factor (CRF) is a potent adrenocorticotropin (ACTH) secretagogue in the mouse pituitary tumor cell strain AtT20/D16v (D16). In the absence of added calcium in the incubation medium a dose of 5 nM CRF stimulates ACTH secretion 2-fold over control values while at medium calcium concentrations greater than 1 mM the same dose of CRF elicits a 3-fold stimulation. In the presence of EGTA or of the calcium antagonists verapamil, cobalt, or lanthanum the CRF effect is abolished. Depolarizing concentrations of extracellular K+ lead to a rapid increase in cell-associated calcium, a response which is inhibited by the dihydropyridine calcium antagonist nimodipine. Although treatment with CRF does not alter the concentration of cell-associated calcium in D16 cells, ACTH secretion stimulated by both CRF and elevated medium K+ are inhibited by nimodipine in a dose-related manner. The results indicate that D16 cells possess both voltage-sensitive and CRF-activated calcium channels.

摘要

合成促肾上腺皮质激素释放因子(CRF)是小鼠垂体肿瘤细胞系AtT20/D16v(D16)中一种有效的促肾上腺皮质激素(ACTH)促分泌素。在孵育培养基中不添加钙的情况下,5 nM的CRF剂量可使ACTH分泌比对照值增加2倍,而在培养基钙浓度大于1 mM时,相同剂量的CRF可引起3倍的刺激。在存在乙二醇双四乙酸(EGTA)或钙拮抗剂维拉帕米、钴或镧的情况下,CRF的作用被消除。去极化浓度的细胞外钾离子会导致细胞相关钙的快速增加,这种反应被二氢吡啶钙拮抗剂尼莫地平抑制。尽管用CRF处理不会改变D16细胞中细胞相关钙的浓度,但CRF和升高的培养基钾离子刺激的ACTH分泌均被尼莫地平以剂量相关的方式抑制。结果表明,D16细胞同时具有电压敏感性钙通道和CRF激活的钙通道。

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