The mechanism of malignant hyperthermia involves an excessive opening of the ryanodine receptor channel, with massive...

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The mechanism of malignant hyperthermia involves an excessive opening of the ryanodine receptor channel, with massive release of Ca2+ from the sarcoplasmic reticulum into the cytosol of skeletal muscle cells. The rate of Ca²+ release is so great that sarcoplasmic reticulum Ca2+-ATPase pumps are unable to work fast enough to re-sequester it. Review the steps in muscle contraction with attention to Ca²+ handling by dragging each step of muscle contraction given at left to the proper position depicted in the figure. Rising intracellular levels of Ca²+ facilitate binding to troponin and opening of myosin binding sites. Action potential cessation in the sarcolemma allows Ca²+-ATPase pumps to re-sequester Ca²+ in the SR. Voltage sensors in the T- tubule mechanically activate ryanodine receptors in the terminal cisternae. Cross-bridge formation and cycling in the continued presence of ATP and Ca²+ generates tension. Decreasing cytosolic Ca²+ levels cause unbinding from troponin and restoration of blocked myosin binding sites. Action potentials traveling along the sarcolemma arrive at and continue along and into the T-tubules. Reset The mechanism of malignant hyperthermia involves an excessive opening of the ryanodine receptor channel, with massive release of Ca2+ from the sarcoplasmic reticulum into the cytosol of skeletal muscle cells. The rate of Ca²+ release is so great that sarcoplasmic reticulum Ca2+-ATPase pumps are unable to work fast enough to re-sequester it. Review the steps in muscle contraction with attention to Ca²+ handling by dragging each step of muscle contraction given at left to the proper position depicted in the figure. Rising intracellular levels of Ca²+ facilitate binding to troponin and opening of myosin binding sites. Action potential cessation in the sarcolemma allows Ca²+-ATPase pumps to re-sequester Ca²+ in the SR. Voltage sensors in the T- tubule mechanically activate ryanodine receptors in the terminal cisternae. Cross-bridge formation and cycling in the continued presence of ATP and Ca²+ generates tension. Decreasing cytosolic Ca²+ levels cause unbinding from troponin and restoration of blocked myosin binding sites. Action potentials traveling along the sarcolemma arrive at and continue along and into the T-tubules. Reset

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Answer Steps in order 1 Action potentials traveling along the ... View the full answer