[The effect of calcitonin on contractile function of skeletal muscles (author's transl)]

The analgesic effect of calcitonin in osteoporosis has been considered to originate from its actions on bone metabolism. However, the author assumed a possible presence of other mechanism, since the analgesic effect of calcitonin manifests in an extremely early phase in which an increase in bone mass is hardly conceivable. Namely, the author postulated that its analgesic effect is due to its actions on body trunk muscles, and investigated experimentally the effect of calcitonin on skeletal muscles. The following results were obtained. 1) Recovery from decreased twitch contraction of M. triceps surae was shown in vivo in rats treated with calcitonin, with dose-response relationship. 2) Calcitonin exerted no effect on partial blockade by dTc, in neuro-muscular junction. Therefore, the neuro-muscular junction is probably not the site of the actions of calcitonin. 3. In an in vitro study on isolated M. soleus, the decrease contraction was recovered after treatment with calcitonin. A correlation was found between this recovery and the dose of calcitonin. 4) In the calcitonin treated muscle, a pronounced persistence of normal contraction was demonstrated in contrast to the control group. 5) Calcitonin appears to facilitate Ca release through exerting actions on Ca transport system in the sarcoplasmic reticulum. From these results, it was shown that calcitonin appears to possess an activity to elevate contractile ability of skeletal muscles. This activity is considered to be derived from its effect on sarcoplasmic reticulum. This activity of calcitonin on contractile function of skeletal muscles indicates the presence of a mechanism relating to skeletal muscles in the analgesic effect on low back pain in osteoporosis.