Wang X B, Sato N, Greer M A
Department of Medicine, Oregon Health Sciences University, Portland 97201.
Mol Cell Endocrinol. 1992 Jan;83(1):79-84. doi: 10.1016/0303-7207(92)90198-f.
Medium hyperosmolarity between 300 (normal medium osmolarity) and 600 mOsm inhibited in a concentration-correlated fashion (r greater than 0.97, p less than 0.001) the rise in intracellular Ca2+ concentration ([Ca2+]i) and prolactin (PRL) secretion induced in GH4C1 cells by depolarizing 30 mM K+. [Ca2+]i concentration and PRL secretion were tightly related between 300 and 600 mOsm (r = 0.976, p less than 0.001); 50% inhibition of both occurred at 450 mOsm. Medium hyperosmolarity slowed the rate of Ca2+ influx. At 600 mOsm the rise in both [Ca2+]i and PRL secretion was abolished but PRL secretion induced by 1 microM phorbol 12-myristate 13-acetate was not significantly reduced. Our data suggest that inhibition of Ca2+ influx may be the primary mechanism by which extracellular hyperosmolarity inhibits PRL secretion induced by high medium K+ in GH4C1 cells. Depression of the Ca2+ intracellular transduction system may play a pathophysiological role in vivo in conditions such as dehydration and hypertonic coma.
介于300(正常培养基渗透压)和600毫渗摩尔之间的中等高渗以浓度相关的方式(r大于0.97,p小于0.001)抑制了30 mM K⁺去极化诱导的GH4C1细胞内细胞内Ca²⁺浓度([Ca²⁺]i)升高和催乳素(PRL)分泌。在300至600毫渗摩尔之间,[Ca²⁺]i浓度和PRL分泌密切相关(r = 0.976,p小于0.001);两者在450毫渗摩尔时均受到50%的抑制。培养基高渗减缓了Ca²⁺内流速率。在600毫渗摩尔时,[Ca²⁺]i升高和PRL分泌均被消除,但1 microM佛波醇12 -肉豆蔻酸酯13 -乙酸酯诱导的PRL分泌没有显著降低。我们的数据表明,Ca²⁺内流的抑制可能是细胞外高渗抑制GH4C1细胞中高培养基K⁺诱导的PRL分泌的主要机制。Ca²⁺细胞内转导系统的抑制在体内诸如脱水和高渗性昏迷等情况下可能发挥病理生理作用。