Scherübl H, Raue F, Zopf G, Hoffmann J, Ziegler R
Department of Internal Medicine, University of Heidelberg, F.R.G.
Mol Cell Endocrinol. 1989 May;63(1-2):263-6. doi: 10.1016/0303-7207(89)90103-2.
The extracellular ionized calcium concentration (Ca2+) is a main regulator of calcitonin (CT) release. Calcium-induced CT secretion differs for acute versus long-term alterations of Ca2+. Using the rat C cell line rMTC 6-23 we have investigated the effect of repetitive stimulation by Ca2+ on CT release. After a Ca-induced initial rise of CT secretion, repetitive Ca stimulation led to a decline of CT release to unstimulated levels (after about 4 h). Reversing the high Ca2+ concentration (2.0 mM) to basal (1.1 mM) for 2 h and then increasing Ca2+ again resulted in a restored stimulatory action of Ca2+ (about 100% increase above the control). In contrast, repetitive stimulation with the dihydropyridine Ca channel agonist Bay K-8644 showed an unchanged stimulatory effect, as observed for the cAMP analog 8-bromo-cAMP, too. The results indicate that the reversible desensitization of Ca-induced CT secretion might be due to a modification of the voltage-dependent Ca channels proximal to or at the site of Bay K-8644 action.
细胞外游离钙浓度（Ca2+）是降钙素（CT）释放的主要调节因子。钙诱导的CT分泌在Ca2+的急性与长期改变方面存在差异。我们使用大鼠C细胞系rMTC 6-23研究了Ca2+重复刺激对CT释放的影响。在钙诱导CT分泌出现初始升高后，重复的钙刺激导致CT释放降至未刺激水平（约4小时后）。将高钙浓度（2.0 mM）恢复至基础浓度（1.1 mM）2小时，然后再次升高Ca2+，导致Ca2+的刺激作用恢复（比对照增加约100%）。相比之下，用二氢吡啶类钙通道激动剂Bay K-8644进行重复刺激显示出不变的刺激作用，环磷酸腺苷类似物8-溴环磷酸腺苷也观察到同样的情况。结果表明，钙诱导的CT分泌的可逆脱敏可能是由于在Bay K-8644作用位点近端或该位点处的电压依赖性钙通道发生了改变。
