Wang X B, Sato N, Greer M A, Greer S E, McAdams S
Department of Medicine, Oregon Health Sciences University, Portland.
Acta Endocrinol (Copenh). 1990 Aug;123(2):218-24. doi: 10.1530/acta.0.1230218.
The mechanism by which 30% medium hyposmolarity induces PRL secretion by GH4C1 cells was compared with that induced by 100 nmol/l TRH or 30 mmol/l K+. Removing medium Ca2+, blocking Ca2+ channels with 50 mumol/l verapamil, or inhibiting calmodulin activation with 20 mumol/l trifluoperazine, 10 mumol/l chlorpromazine or 10 mumol/l pimozide almost completely blocked hyposmolarity-induced secretion. The smooth muscle relaxant, W-7, which is believed relatively specific in inhibiting the Ca2(+)-calmodulin interaction, depressed hyposmolarity-induced PRL secretion in a dose-dependent manner (r = -0.991, p less than 0.01). The above drugs also blocked or decreased high K(+)-induced secretion, but had much less effect on TRH-induced secretion. Secretion induced by TRH, hyposmolarity, or high K+ was optimal at pH 7.3-7.65 and was significantly depressed at pH 6.0 or 8.0, indicating that release of hormone induced by all 3 stimuli is due to an active cell process requiring a physiologic extracellular pH and is not produced by nonspecific cell toxicity. The data suggest hyposmolarity and high K+ may share some similarities in their mechanism of stimulating secretion, which is different from that of TRH.
将30%的低渗培养基诱导GH4C1细胞分泌催乳素（PRL）的机制与100 nmol/l促甲状腺激素释放激素（TRH）或30 mmol/l钾离子（K+）诱导的机制进行了比较。去除培养基中的钙离子（Ca2+）、用50 μmol/l维拉帕米阻断钙离子通道或用20 μmol/l三氟拉嗪、10 μmol/l氯丙嗪或10 μmol/l匹莫齐特抑制钙调蛋白激活，几乎完全阻断了低渗诱导的分泌。平滑肌松弛剂W-7被认为在抑制Ca2(+)-钙调蛋白相互作用方面相对特异，它以剂量依赖的方式抑制低渗诱导的PRL分泌（r = -0.991，p < 0.01）。上述药物也阻断或减少了高钾诱导的分泌，但对TRH诱导的分泌影响小得多。TRH、低渗或高钾诱导的分泌在pH 7.3 - 7.65时最佳，在pH 6.0或8.0时显著降低，这表明所有这三种刺激诱导的激素释放是由于一个需要生理细胞外pH的活跃细胞过程，而不是由非特异性细胞毒性产生的。数据表明，低渗和高钾在刺激分泌的机制上可能有一些相似之处，这与TRH的机制不同。
