In cardiac muscle cells, what process links an action potential to muscle contraction?
Potassium efflux and membrane repolarization
Inhibition of myosin heads
Closing of sodium channels
Calcium entry and activation of contractile proteins
The Correct Answer is D
A. Potassium efflux and membrane repolarization: Potassium efflux occurs during the repolarization phase of the cardiac action potential, restoring the resting membrane potential. While necessary for resetting the cell electrically, it does not directly trigger the contractile machinery or link the action potential to muscle contraction.
B. Inhibition of myosin heads: Myosin head inhibition occurs when tropomyosin blocks binding sites on actin in relaxed muscle. This is the resting state prior to contraction, not the process that couples the action potential to contraction.
C. Closing of sodium channels: Sodium channels close immediately after depolarization, contributing to the refractory period and preventing further Na+ influx. While important for the timing of action potentials, this does not directly initiate contraction or activate contractile proteins.
D. Calcium entry and activation of contractile proteins: During excitation-contraction coupling in cardiac muscle, calcium ions enter the cell through voltage-gated L-type calcium channels during the plateau phase. This calcium triggers release of Ca2+ from the sarcoplasmic reticulum, allowing calcium to bind to troponin. Troponin undergoes a conformational change, which permits myosin cross-bridge cycling ultimately producing muscle contraction.
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Related Questions
Correct Answer is A
Explanation
A. Atrial cells have a resting potential of -80 mV, while ventricular cells have a resting potential of -90 mV: Cardiac contractile cells maintain a negative resting membrane potential due to selective permeability to potassium ions and the activity of the Na+/K+ ATPase pump. Atrial myocytes have a resting potential around -80 mV, while ventricular myocytes are slightly more negative at approximately -90 mV.
B. Both atrial and ventricular cells have a resting potential of -70 mV: A resting potential of -70 mV is characteristic of neurons, not cardiac contractile cells. Cardiac myocytes require a more negative resting potential to maintain proper excitability and ensure effective action potential generation for coordinated contraction.
C. Atrial cells have a resting potential of -90 mV, while ventricular cells have a resting potential of -80 mV: This reverses the actual values of atrial and ventricular cells. Ventricular cells are more polarized than atrial cells at rest due to higher potassium conductance and greater expression of inward-rectifier potassium channels.
D. Both atrial and ventricular cells have a resting potential of -60 mV: A resting potential of -60 mV is typical of pacemaker (autorhythmic) cells, such as those in the sinoatrial node, rather than contractile myocytes. Contractile cells require a more negative resting potential to maintain a stable resting state before depolarization.
Correct Answer is B
Explanation
A. Weaker contractions: Within normal physiological limits, increasing ventricular stretch does not weaken contractions. Weak contractions may occur only if the muscle is overstretched beyond its optimal sarcomere length, which exceeds the Frank-Starling range.
B. Enhanced force of contraction: The Frank-Starling law of the heart states that increased ventricular filling stretches myocardial fibers, optimizing actin-myosin overlap within sarcomeres. This enhanced sarcomere alignment increases the force of contraction during systole, allowing the heart to eject a greater stroke volume in response to increased venous return.
C. Reduced stroke volume: Increasing ventricular preload within physiological limits actually increases stroke volume by enhancing contractile force. Stroke volume only decreases if the heart is overfilled beyond its optimal sarcomere length, leading to inefficient contraction.
D. Decreased venous return: Increasing ventricular stretch is a response to increased venous return, not a cause of decreased return. Venous return drives end-diastolic volume, which in turn stretches the ventricular muscle to regulate stroke volume according to the Frank-Starling mechanism.
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