Abstract
Two second messengers, cyclic ADP-ribose (cADPR) and inositol 1,4,5-trisphosphate (IP3), potentiated the Ca2+release from sarcoplasmic reticulum induced by transverse tubular membrane depolarization monitored in a triadic vesicle prepared from skeletal muscle. However, without depolarization they could not trigger the Ca2+release. On the contrary, only cADPR potentiated caffeine-induced Ca2+release. Because Ca2+releases potentiated by cADPR and IP3were inhibited by 1 μM ruthenium red and 100 μM ryanodine, probably these second messengers potentiated the Ca2+release through ryanodine receptor Ca2+channels. These results suggest that in skeletal excitation-contraction coupling, cADPR and IP3play a role as a potentiator or a modifierin vivo,but both modification pathways are different from each other.
Published Version
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