Aragno R, Bettini V, Fabro P, Ton P, Munari L, Munari P F
Farmaco Sci. 1986 Jul;41(7):523-9.
Previous observations had shown that, in the isolated rat preparations, calcitonin facilitates the excitement transmission from autonomic nerve-endings to smooth muscle. The present research, was designed to verify whether this facilitation effect could be present in somatic nerve-endings too. For this reason, we used the isolated frog "sciatic nerve-gastrocnemius muscle" preparation where the calcitonin influence on the beginning of a complete tetanic response was studied. The motor nerve-endings were stimulated at different frequencies. It was observed that the added calcitonin and/or an increased [Ca++] medium induced a complete tetanic response also at stimulating frequencies that, in the controls, provoked only a clonic response. Moreover, both the calcitonin and the increased [Ca++] medium frequently induced an increase in the mechanical muscle tension developed. These facilitating effects were reduced or even abolished with inhibition of Ca++-passage through the cell membrane by nifedipine. Therefore, we could hypothesize that the added calcitonin causes increased Ach-release from the somatic nerve-endings and that this action depends on facilitated Ca++-passage through the cell membrane of the nerve-endings and of the muscle fibres too.
先前的观察表明,在离体大鼠标本中,降钙素可促进自主神经末梢至平滑肌的兴奋传递。本研究旨在验证这种促进作用在躯体神经末梢中是否也存在。因此,我们使用了离体青蛙“坐骨神经-腓肠肌”标本,研究降钙素对完全强直反应起始的影响。以不同频率刺激运动神经末梢。观察到,添加降钙素和/或增加培养基中的[Ca++]浓度后,在对照组中仅引发阵挛性反应的刺激频率下,也能诱导出完全强直反应。此外,降钙素和增加的[Ca++]培养基均频繁诱导肌肉产生的机械张力增加。通过硝苯地平抑制Ca++通过细胞膜后,这些促进作用减弱甚至消失。因此,我们可以推测,添加的降钙素会导致躯体神经末梢释放的乙酰胆碱增加,且这种作用也依赖于促进Ca++通过神经末梢和肌肉纤维的细胞膜。