DHPR subunit

It is now widely believed that in skeletal muscle a depolarization-induced change in the structure of the DHPR a 1 subunit directly influences the RyR in such a way as to markedly increase its conductance for Ca +. Since the resulting increase in [Ca +]i can open other RyR channels, this produces a surge of Ca + release. In contrast, cardiac muscle expresses a different a 1 DHPR subunit than skeletal muscle. The cardiac subunit has much higher channel conductance and faster kinetics than the skeletal muscle type, and so admits much more extracellular calcium during the action potential. Thus, CICR does play an important role in cardiac muscle. In both cases, high [Ca +]i reduces RyR conductance, by direct binding of Ca + (or Ca +-calmodulin) to RyR, by activation of a kinase that phosphorylates RyR, and probably both. At the same time, Ca-calmodulin (Ca-CaM) activates a protein kinase that phosphorylates the SR Ca-ATPase, which increases its activity 10- to 100-fold. These two mechanisms combine to terminate the Ca " " spike. 

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