Spada A, Reza-Elahi F, Lania A
Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS, Milano, Italy.
J Endocrinol Invest. 1990 Jan;13(1):13-8. doi: 10.1007/BF03348570.
The effect of TRH on cytosolic free calcium concentrations, [Ca2+]i, was evaluated on cell suspensions obtained from 6 human PRL secreting pituitary adenomas. In these cells resting [Ca2+]i levels were variable (mean +/- SE; 103.8 +/- 6.5, n = 25); the addition of 100 nM TRH caused a marked [Ca2+]i rise within 20 sec., the peak values ranging from 200 to 437 nM (285 +/- 10.8 nM, n = 10). The transients induced by TRH were composed by a rapid increase, due to mobilization of calcium from intracellular stores, followed within a few seconds by a lower plateau which was due to stimulated influx from the extracellular space. In fact, when EGTA and verapamil were applied after TRH they caused the Ca2+ plateau to dissipate rapidly. The addition of 1 microM dopamine (DA) caused a substantial decrease of resting [Ca2+]i (about 10-30%) as well as an inhibition of the plateau phase induced by TRH. The effect of DA completely depended on extracellular Ca2+. The TRH-induced transients observed in adenomatous cells were quite similar in size and time course to those recorded in normal rat lactotrophs. As previously observed in rat lactotrophs, in adenomatous cells treatment with pertussis toxin (PTx, 1 microgram/ml for 4 h) was unable to affect the [Ca2+]i transients induced by TRH while completely abolished the effect of DA. The effects of TRH on in vivo and in vitro PRL secretion were also evaluated. Before surgery, no patient showed a positive response to the iv administration of 200 micrograms TRH (serum PRL levels: 95 +/- 62 ng/ml in basal conditions vs 124 +/- 92 after TRH, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
在从6例分泌催乳素的人垂体腺瘤中获取的细胞悬液上评估促甲状腺激素释放激素（TRH）对胞质游离钙浓度[Ca2+]i的影响。在这些细胞中，静息[Ca2+]i水平各不相同（均值±标准误；103.8±6.5，n = 25）；添加100 nM TRH后，[Ca2+]i在20秒内显著升高，峰值范围为200至437 nM（285±10.8 nM，n = 10）。TRH诱导的瞬变由快速升高组成，这是由于细胞内钙库中钙的动员，随后在几秒钟内出现较低的平台期，这是由于细胞外空间钙内流增加所致。事实上，在TRH作用后应用乙二醇双四乙酸（EGTA）和维拉帕米会导致Ca2+平台期迅速消失。添加1 μM多巴胺（DA）会使静息[Ca2+]i大幅降低（约10% - 30%），并抑制TRH诱导的平台期。DA的作用完全依赖于细胞外钙。在腺瘤细胞中观察到的TRH诱导的瞬变在大小和时间进程上与正常大鼠催乳素细胞中记录的非常相似。如先前在大鼠催乳素细胞中所观察到的，在腺瘤细胞中用百日咳毒素（PTx，1 μg/ml处理4小时）不能影响TRH诱导的[Ca2+]i瞬变，而完全消除了DA的作用。还评估了TRH对体内和体外催乳素分泌的影响。手术前，没有患者对静脉注射200 μg TRH表现出阳性反应（血清催乳素水平：基础状态下为95±62 ng/ml，TRH注射后为124±92 ng/ml，P = 无显著差异）。（摘要截断于250字）
