Quiz 13: Cardiac Muscle

Contraction of cardiac muscle typically requires: A)Ca⁺⁺ influx through voltage-gated Ca⁺⁺ channels to trigger a rise in cytosolic [Ca⁺⁺]. B)Ca⁺⁺ influx through voltage-gated Ca⁺⁺ channels,which is sufficient to support contraction. C)Activation of myosin light-chain kinase (MLCK). D)Phosphorylation of myosin heavy chain. E)Ca⁺⁺ influx through the Na⁺-Ca⁺⁺ antiporter.

Relaxation of cardiac muscle typically requires: A)Myosin light-chain dephosphorylation. B)Activation of the ryanodine receptor. C)Ca⁺⁺ uptake by the sarcoplasmic reticulum (SR). D)Phosphorylation of phospholamban. E)Activation of the dihydropyridine receptor.

The force of contraction of cardiac muscle is typically increased by: A)An increase in Ca⁺⁺ extrusion by the Na⁺-Ca⁺⁺ antiporter in cardiac muscle. B)An increase in myosin phosphorylation in cardiac muscle. C)A decrease in cytosolic [Ca⁺⁺] in the cardiac muscle. D)β-Adrenergic stimulation of the cardiac muscle. E)Recruitment of more cardiac muscle cells.

Epinephrine increases the force of contraction of cardiac muscle by: A)Increasing the amount of Ca⁺⁺ in the SR for release to the cytosol. B)Increasing the level of myosin light-chain phosphorylation. C)Inhibiting the ryanodine receptor. D)Increasing Ca⁺⁺ extrusion through the sarcolemmal Ca⁺⁺ pump. E)Shortening the duration of the action potential.

Stretching cardiac muscle results in an increase in the force of contraction as a result of: A)Activation of K⁺ channels. B)An increase in the sensitivity of actin-myosin interactions to Ca⁺⁺. C)Phosphorylation of the ryanodine receptor. D)Increased phosphorylation of troponin I. E)Increased Ca⁺⁺ influx through the Na⁺-Ca⁺⁺ antiporter.

Calsequestrin in cardiac muscle: A)Acts as a high-affinity Ca⁺⁺ buffer in the cytosol. B)Acts as a low-affinity Ca⁺⁺ buffer in the SR lumen,near the ryanodine receptor. C)Promotes Ca⁺⁺ accumulation by the mitochondria. D)Increases the Ca⁺⁺ affinity of the sarcolemmal Ca⁺⁺ pump. E)Facilitates myosin binding to the actin thin filament.

Cardiac muscle cells in the atria are capable of contracting spontaneously because of a spontaneous depolarization that results from: A)An inward current through a hyperpolarization-activated channel. B)Cyclic changes in the activity of Na⁺,K⁺-ATPase. C)Slow leak of Ca⁺⁺ through the dihydropyridine receptor. D)Cyclic changes in the activity of the sarcolemmal Ca⁺⁺ pump. E)Cyclic changes in the activity of SERCA.

Mutations in the cardiac ryanodine receptor have been associated with cardiac arrhythmias.Specifically,a mutation in the cardiac ryanodine receptor that increases Ca⁺⁺ efflux from the SR promotes the development of delayed afterdepolarizations by: A)Decreasing the activity of calcineurin. B)Increasing Ca⁺⁺ efflux through the Na⁺-Ca⁺⁺ antiporter. C)Increasing mitochondrial Ca⁺⁺ uptake. D)Decreasing actin-myosin interactions. E)Increasing the activity of K⁺ channels.

The mechanisms underlying the development of cardiac hypertrophy are complex,although relaxation abnormalities that result in chronic elevation of cytosolic Ca⁺⁺ level appear to promote the development of hypertrophy through: A)Stimulation of the sarcolemmal Ca⁺⁺ pump. B)Ca⁺⁺ binding to troponin I. C)Activation of calcineurin. D)Inhibition of Ca⁺⁺/calmodulin-dependent protein kinase. E)Opening of Ca⁺⁺-activated K⁺ channels.