As the sarcoplasmic reticulum is the main storage site of Ca2+, and as caffeine has been shown to produce contractures in malignant-hyperthermia-susceptible muscle at much lower concentrations than in normal muscle, most experimental work has focused on the role of the sarcoplasmic reticulum in the pathophysiology of malignant hyperthermia.
Calcium is stored with calsequestrin in the terminal cisternas of the sarcoplasmic reticulum; it is released on depolarization and taken up again by means of an ATP-dependent Ca2+ pump. It has been shown that an increase in sarcoplasmic Ca2+ can itself cause release of further Ca2+, a process known as Ca2+-induced Ca2+ release. Although the role of this process in normal physiology is questionable, it has been postulated as a mechanism for malignant hyperthermia. Other studies of the sarcoplasmic reticulum suggest that a defect in the control of Ca2+ efflux from the sarcoplasmic reticulum may cause malignant hyperthermia.
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