29) Excitation-contraction coupling in skeletal muscle involves ALL of the follo

Question

29) Excitation-contraction coupling in skeletal muscle involves ALL of the following events except one. Which one is NOT involved?

A) ATP hydrolysis

B) Binding of Ca2+ to calmodulin

C) Depolarization of the sarcolemma

D) Cross-bridge cycling

30) Malignant hyperthermia is a potentially fatal genetic disorder characterized by a hyperresponsiveness to anesthetics, which results in elevated body temperature, and skeletal muscle contractions. Which of the following could account for these clinical manifestations?

A) Inhibition of the ryanodine receptor (RYR) channels

B) Prolonged opening of the ryanodine receptor (RYR) channels

C) Enhanced activity of the sarcoplasmic reticulum Ca2+ ATPase (SERCA)

D) Reduction in the density of voltage-gated Na+ channels in the T-tubule membrane

31) Administration of which of the following would reverse the effects of a non-depolarizing muscle blocker on the neuromuscular junction?

A) Na+ channel blocker

B) Acetylcholine receptor antagonist

C) Reversible acetylcholinesterase inhibitor

D) Inhibitor of excitation-contraction coupling

Explanation / Answer

29)

Excitation-contraction coupling in skeletal muscle involves ALL of the following events except cross-bridge cycling. Option D is correct. The ATP hydrolysis takes place when the myosin binds with actin during contraction. The ER of sarcolemma releases Ca2+ ions that bind to calmodulin at sarcolemma surface. Thus, the sarcolemma is depolarised.

30)

Malignant hyperthermia is characterised by the clinical manifestation such as prolonged opening of the ryanodine receptor (RYR) channels. As long as the ryanodine receptors are opened the influx of the calcium ions from sarcoplasmic reticulum to sarcoplasm is continued stimulating muscle contraction. Prolonged muscle contraction generates more heat and causes lactic acidosis and muscle rigidity. Hence, option B os correct.

31)

Administration of Acetylcholine receptor antagonist would reverse the effects of a non-depolarizing muscle blocker on the neuromuscular junction. Option B is correct. This is because nondepolarizing blockers compete with Acetyl choline receptors and the blockade can be reversed by increasing the concentra tion of acetyl choline receptors but intensified, by administration of acetylcholine inhibitors.

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