[Mechanisms and their pharmacology of mobilization of calcium ion in muscle cells].

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.