Scherubl H, Raue F, Hoflich M, Ziegler R
Henry Ford Hosp Med J. 1989;37(3-4):198-200.
Voltage-dependent calcium channels (VDCC) regulating Ca++ influx through the cellular plasma membrane play a major role in the Ca(++)-induced calcitonin (CT) secretion. Using rat C-cells (rMTC 6-23 cell line), we have studied the effect of repetitive stimulation by either Ca++ (2 mM) or glucagon (10 microM) or epinephrine (10 microM) on CT secretion. Following a Ca(++)-induced initial rise, CT release declined to basal levels after about four hours despite high Ca++; addition of 10 microM glucagon to the "Ca++ desensitized C-cells" yielded the normal stimulatory effect of glucagon on CT release. Repetitive stimulation with glucagon showed a constant stimulatory action over an eight-hour period. In contrast, repetitive stimulation with 10 microM epinephrine caused an initial rise followed by a gradual decline of CT release over six hours. The observed desensitization of Ca(++)-induced CT secretion may be due to a modification of VDCC in C-cells. Whether or not the desensitization of epinephrine-induced CT release occurs independently of the regulation of VDCC remains unclear.
电压依赖性钙通道（VDCC）通过细胞膜调节钙离子内流，在钙离子诱导的降钙素（CT）分泌中起主要作用。利用大鼠C细胞（rMTC 6 - 23细胞系），我们研究了用钙离子（2 mM）、胰高血糖素（10 microM）或肾上腺素（10 microM）重复刺激对CT分泌的影响。在钙离子诱导的初始升高后，尽管钙离子浓度较高，但约4小时后CT释放降至基础水平；向“钙离子脱敏的C细胞”中添加10 microM胰高血糖素，产生了胰高血糖素对CT释放的正常刺激作用。用胰高血糖素重复刺激在8小时内显示出持续的刺激作用。相比之下，用10 microM肾上腺素重复刺激导致CT释放在6小时内先升高后逐渐下降。观察到的钙离子诱导的CT分泌脱敏可能是由于C细胞中VDCC的改变。肾上腺素诱导的CT释放脱敏是否独立于VDCC的调节尚不清楚。
