Sato N, Wang X, Greer M A
Department of Medicine, Oregon Health Sciences University, Portland 97201.
Mol Cell Endocrinol. 1991 May;77(1-3):193-8. doi: 10.1016/0303-7207(91)90074-3.
We studied the influence of graded degrees of hyperosmolarity on the dynamics of the thyrotropin-releasing hormone (TRH)-induced rise in cytosol Ca2+ concentration ([Ca2+]i) and prolactin (PRL) secretion in GH4C1 cells. TRH caused two phases of increase in [Ca2+]i that were differentially altered by hyperosmolarity: 100% hyperosmolarity (600 mOsm) depressed only 20% of an initial high-amplitude [Ca2+]i burst (first phase) dependent on Ca2+ mobilized from intracellular pools, but it abolished a sustained low-amplitude second phase dependent on extracellular Ca2+ influx. Low degrees of hyperosmolarity suppressed PRL secretion due to Ca2+ influx while high degrees suppressed secretion due to mobilized Ca2+. These data suggest that in GH4C1 cells hypertonic inhibition of secretion may result from both blocking Ca2+ influx and mechanisms unrelated to [Ca2+]i.
我们研究了不同程度的高渗对促甲状腺激素释放激素(TRH)诱导的GH4C1细胞胞质Ca2+浓度([Ca2+]i)升高及催乳素(PRL)分泌动力学的影响。TRH引起[Ca2+]i升高的两个阶段,高渗对其有不同改变:100%高渗(600 mOsm)仅抑制了依赖于从细胞内钙库动员的Ca2+的初始高幅度[Ca2+]i爆发(第一阶段)的20%,但消除了依赖于细胞外Ca2+内流的持续低幅度第二阶段。低程度的高渗抑制由于Ca2+内流引起的PRL分泌,而高程度的高渗抑制由于动员的Ca2+引起的分泌。这些数据表明,在GH4C1细胞中,高渗对分泌的抑制可能是由于阻断Ca2+内流以及与[Ca2+]i无关的机制所致。