Yamashita N, Takano K, Teramoto A, Tatakura K, Ogata E
Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.
Endocrinol Jpn. 1992 Oct;39(5):491-7. doi: 10.1507/endocrj1954.39.491.
Changes in the membrane potential and the intracellular Ca2+ concentration ([Ca2+]i) caused by somatostatin (SRIF) were simultaneously measured in human GH-producing pituitary tumor cells, by means of the nystatin-perforated whole cell clamp technique and Fura-2 AM. An application of 10(-8) M SRIF hyperpolarized the membrane and arrested Ca(2+)-dependent spontaneous action potentials. [Ca2+]i concurrently decreased during membrane hyperpolarization. When the membrane potential was clamped below the threshold for voltage-gated Ca2+ channels, [Ca2+]i decreased and SRIF did not further reduce [Ca2+]i. In cells which did not show spontaneous action potentials, SRIF hyperpolarized the membrane but it affected [Ca2+]i little. From these results it was concluded that the reduction in [Ca2+]i caused by SRIF was ascribed to the decrease in Ca2+ influx through voltage-gated channels during membrane hyperpolarization. The effect of SRIF on the voltage-gated Ca2+ channel current was also examined under the perforated whole cell clamp. SRIF (10(-8) M) inhibited the Ca2+ channel current to 80.8 +/- 15.4% (n = 5) of the control. Because SRIF-induced inhibition of the voltage-gated Ca2+ channel current was not prominent, it was considered that membrane hyperpolarization is the major cause of the reduction in [Ca2+]i in human GH-producing cells.
利用制霉菌素穿孔全细胞钳技术和Fura-2 AM，同时测量了生长抑素（SRIF）对人垂体生长激素瘤细胞的膜电位和细胞内Ca2+浓度（[Ca2+]i）的影响。施加10(-8) M的SRIF可使细胞膜超极化，并抑制Ca(2+)依赖性自发动作电位。在细胞膜超极化过程中，[Ca2+]i同时降低。当膜电位钳制在电压门控Ca2+通道阈值以下时，[Ca2+]i降低，且SRIF不会进一步降低[Ca2+]i。在未表现出自发动作电位的细胞中，SRIF使细胞膜超极化，但对[Ca2+]i影响很小。从这些结果可以得出结论，SRIF引起的[Ca2+]i降低归因于膜超极化过程中通过电压门控通道的Ca2+内流减少。在穿孔全细胞钳条件下，还研究了SRIF对电压门控Ca2+通道电流的影响。SRIF（10(-8) M）将Ca2+通道电流抑制至对照的80.8 +/- 15.4%（n = 5）。由于SRIF对电压门控Ca2+通道电流的抑制作用不显著，因此认为膜超极化是导致人垂体生长激素瘤细胞中[Ca2+]i降低的主要原因。
