筋細胞におけるカルシウム・イオン動員機構とその薬理

抄録

Mechanisms and their pharmacology of Ca ion mobilization in skeletal, cardiac and smooth muscles are reviewed. In skeletal muscle, it is very likely that depolarization of T-tubule membrane causes conformational changes of dihydropyridine (DHP) receptors in the T-membrane, which in turn, most probably through some kind of protein-protein interaction, open the Ca²⁺ release channel in the sarcoplasmic reticulum (SR), the ryanodine receptor. Both the DHP receptor and ryanodine receptor have already been purified and sequenced, but the nature of the information transduction between these proteins still remains to be solved. Both of these proteins appear to have dual functions : the DHP receptor as a voltage sensor as described above and as a voltage-dependent Ca²⁺ channel and the ryanodine receptor as a physiological Ca²⁺ release channel and as a Ca²⁺-induced Ca²⁺ release (CICR) channel, an abnormality of which is known to cause malignant hyperthermia. In cardiac muscle, Ca²⁺ influx is essential not as the main Ca²⁺ source but to release Ca²⁺ from the SR, probably not through the CICR mechanism in the narrow sense but through a mechanism dependent on both Ca²⁺ and T-tubule depolarization. Several mechanisms of Ca²⁺ mobilization are used in smooth muscles and their features, different from those in striated muscles, are briefly reviewed.