Impaired Calcium Homeostasis and Calcium Antagonists in Muscle Diseases
The electrical excitation of the muscle plasma membrane following a nerve impulse spreads into the T-tubule system. The electrical signal is then transferred to the sarcoplasmic reticulum, and large amounts of Ca2+ stored in its lumen are released into the cytosol. In the resting state at low cytosolic Ca2+ concentrations (about 10−7 M), tropomyosin sterically blocks the interaction of myosin heads with actin. When the cytosolic Ca2+ level is raised up to 10−5 M following the electrical excitation, free Ca2+ interacts with troponin, resulting in a conformational change of the tropomyosin, allowing the myosin heads to interact with actin. Subsequently, the Ca2+ concentrations of the myofibrillar compartment are rapidly restored to the resting level by uptake of Ca2+ into the sarcoplasmic reticulum through the Ca2+-Mg2+ ATPase located in the sarcoplasmic reticulum .
KeywordsSarcoplasmic Reticulum Calcium Antagonist Duchenne Muscular Dystrophy Malignant Hyperthermia Myotonic Dystrophy
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