Sussman K E, Leitner J W, Draznin B
Diabetes. 1987 May;36(5):571-7. doi: 10.2337/diab.36.5.571.
We have assessed the effect of somatostatin on glucose-, potassium-, forskolin-, and dibutyryl cAMP-induced changes in cytosolic free [Ca2+] in normal rat pancreatic islet cells with the new Ca2+ indicator fura 2. The cytosolic free [Ca2+] in islet cells incubated with nonstimulatory concentrations of glucose (30 mg/dl) ranged from 54 to 64 nM. In the presence of extracellular Ca2+ (1 mM), glucose (300 mg/dl) rapidly increased the cytosolic free [Ca2+] to a level of 90-110 nM. In the absence of extracellular Ca2+, glucose failed to increase the cytosolic free [Ca2+], which remained at a level of 55-60 nM. Somatostatin inhibited glucose-induced increases in cytosolic free [Ca2+] in a dose-dependent manner (maximal inhibition was 34%). Half-maximal inhibition was observed at 10(-9) M somatostatin, which correlated well with somatostatin binding to islet cells (Kd = 2.6 X 10(-10) M). Potassium (50 mM) rapidly increased the cytosolic free [Ca2+] to 110-120 nM, and its effect was not influenced by the presence of somatostatin. Forskolin (20 microM) and dibutyryl cAMP (1 mM) rapidly increased cytosolic free Ca2+ both in the presence and absence of extracellular Ca2+. More than 80% of the overall increase in cytosolic free-Ca2+ levels could be accounted for by the mobilization of intracellular Ca2+ stores. Somatostatin effectively blocked the forskolin effect (32% inhibition) but not the dibutyryl cAMP-induced effect. Somatostatin appears to inhibit secretagogue-induced increases in cytosolic free [Ca2+] by interfering with cAMP production and probably with Ca2+ transport across the cell membrane.
我们使用新型钙离子指示剂fura 2评估了生长抑素对正常大鼠胰岛细胞中葡萄糖、钾离子、福斯可林和二丁酰环磷腺苷（dibutyryl cAMP）诱导的胞浆游离钙离子浓度变化的影响。在非刺激浓度葡萄糖（30mg/dl）孵育的胰岛细胞中，胞浆游离钙离子浓度范围为54至64nM。在细胞外钙离子存在（1mM）的情况下，葡萄糖（300mg/dl）迅速将胞浆游离钙离子浓度提高到90 - 110nM。在无细胞外钙离子时，葡萄糖未能增加胞浆游离钙离子浓度，其浓度维持在55 - 60nM。生长抑素以剂量依赖性方式抑制葡萄糖诱导的胞浆游离钙离子浓度升高（最大抑制率为34%）。在生长抑素浓度为10(-9)M时观察到半数最大抑制，这与生长抑素与胰岛细胞的结合情况良好相关（解离常数Kd = 2.6×10(-10)M）。钾离子（50mM）迅速将胞浆游离钙离子浓度提高到110 - 120nM，其作用不受生长抑素存在的影响。福斯可林（20μM）和二丁酰环磷腺苷（1mM）在有或无细胞外钙离子的情况下均迅速增加胞浆游离钙离子浓度。胞浆游离钙离子浓度总体升高的80%以上可归因于细胞内钙离子储存的动员。生长抑素有效阻断了福斯可林的作用（抑制率32%），但未阻断二丁酰环磷腺苷诱导的作用。生长抑素似乎通过干扰环磷腺苷的产生以及可能干扰钙离子跨细胞膜的转运来抑制促分泌剂诱导的胞浆游离钙离子浓度升高。
