Podcast
Questions and Answers
What direct effect does the binding of calcium ions to troponin C have on the actin-myosin interaction in cardiomyocytes?
What direct effect does the binding of calcium ions to troponin C have on the actin-myosin interaction in cardiomyocytes?
- It hydrolyzes ATP, providing the energy needed for myosin to bind to actin.
- It strengthens the bond between tropomyosin and actin, preventing myosin binding.
- It causes tropomyosin to shift, exposing the myosin binding sites on actin. (correct)
- It directly phosphorylates myosin heads, increasing their affinity for actin.
During the cardiac excitation-contraction coupling, what is the primary role of ATP in the myosin-actin interaction?
During the cardiac excitation-contraction coupling, what is the primary role of ATP in the myosin-actin interaction?
- ATP is used to transport calcium ions into the sarcoplasmic reticulum.
- ATP hydrolysis powers the 'power stroke' of the myosin head, sliding actin and myosin filaments past each other. (correct)
- ATP is used to block the binding sites on actin, preventing premature muscle contraction.
- ATP facilitates the initial binding of calcium ions to troponin C.
How do calcium ions facilitate the interaction between actin and myosin filaments in cardiac muscle contraction?
How do calcium ions facilitate the interaction between actin and myosin filaments in cardiac muscle contraction?
- Calcium ions directly bind to myosin, activating its ATPase activity.
- Calcium ions bind to troponin C, initiating a conformational change that exposes myosin-binding sites on actin. (correct)
- Calcium ions bind to tropomyosin, promoting its interaction with actin.
- Calcium ions phosphorylate actin, enhancing its binding affinity for myosin.
What is the consequence of removing calcium ions from the sarcoplasm in cardiac muscle cells?
What is the consequence of removing calcium ions from the sarcoplasm in cardiac muscle cells?
What is the ultimate result of the cyclical binding, sliding, and reattaching of myosin heads on actin filaments in cardiac muscle?
What is the ultimate result of the cyclical binding, sliding, and reattaching of myosin heads on actin filaments in cardiac muscle?
Which characteristic distinguishes pacemaker cells from the majority of other heart cells (cardiomyocytes)?
Which characteristic distinguishes pacemaker cells from the majority of other heart cells (cardiomyocytes)?
How does the arrangement of pacemaker cells and cardiomyocytes contribute to the efficient function of the heart?
How does the arrangement of pacemaker cells and cardiomyocytes contribute to the efficient function of the heart?
What is the significance of the heart functioning as a 'functional syncytium'?
What is the significance of the heart functioning as a 'functional syncytium'?
If the sinoatrial (SA) node fails, what is the most likely immediate consequence for the heart's electrical activity?
If the sinoatrial (SA) node fails, what is the most likely immediate consequence for the heart's electrical activity?
How would a drug that selectively blocks the function of the Purkinje fibers likely affect heart function?
How would a drug that selectively blocks the function of the Purkinje fibers likely affect heart function?
What cellular process is essential for initiating an action potential in a pacemaker cell?
What cellular process is essential for initiating an action potential in a pacemaker cell?
What distinguishes 'automaticity' in the heart?
What distinguishes 'automaticity' in the heart?
How would increasing the resistance in the internodal tracts affect the timing of heart contractions?
How would increasing the resistance in the internodal tracts affect the timing of heart contractions?
What is the primary determinant of changes in membrane potential?
What is the primary determinant of changes in membrane potential?
What is the effect of a depolarization wave moving through the heart?
What is the effect of a depolarization wave moving through the heart?
If depolarization waves occur approximately twice per second, what is the heart rate in beats per minute?
If depolarization waves occur approximately twice per second, what is the heart rate in beats per minute?
During Phase 4 of a pacemaker cell action potential, what is the primary event that occurs?
During Phase 4 of a pacemaker cell action potential, what is the primary event that occurs?
What is the 'funny current' in pacemaker cells primarily caused by?
What is the 'funny current' in pacemaker cells primarily caused by?
What voltage triggers Phase 0 in pacemaker cells?
What voltage triggers Phase 0 in pacemaker cells?
What ion is responsible for the rapid depolarization in Phase 0 of pacemaker cells?
What ion is responsible for the rapid depolarization in Phase 0 of pacemaker cells?
Why do pacemaker cells not have a Phase 1 or Phase 2 during their action potential?
Why do pacemaker cells not have a Phase 1 or Phase 2 during their action potential?
What occurs during Phase 3 of the pacemaker cell action potential?
What occurs during Phase 3 of the pacemaker cell action potential?
How do pacemaker cells influence the rest of the heart?
How do pacemaker cells influence the rest of the heart?
What is the function of myocytes?
What is the function of myocytes?
What differentiates cardiac myocytes from skeletal muscle cells in terms of action potential signals?
What differentiates cardiac myocytes from skeletal muscle cells in terms of action potential signals?
What is the resting membrane potential of a myocyte in Phase 4?
What is the resting membrane potential of a myocyte in Phase 4?
Which of the following best describes the role of HCN channels in pacemaker cells?
Which of the following best describes the role of HCN channels in pacemaker cells?
How does the relative number of potassium ion channels compared to HCN channels impact the membrane potential during Phase 3 of the pacemaker cell action potential?
How does the relative number of potassium ion channels compared to HCN channels impact the membrane potential during Phase 3 of the pacemaker cell action potential?
What is the primary role of gap junctions in cardiac myocytes?
What is the primary role of gap junctions in cardiac myocytes?
The influx of which ion is primarily responsible for the rapid depolarization (Phase 0) of a cardiac myocyte action potential?
The influx of which ion is primarily responsible for the rapid depolarization (Phase 0) of a cardiac myocyte action potential?
What is the 'threshold potential' in the context of cardiac myocyte action potentials, and why is it significant?
What is the 'threshold potential' in the context of cardiac myocyte action potentials, and why is it significant?
Why is the action potential in cardiac myocytes described as an 'all-or-none' process?
Why is the action potential in cardiac myocytes described as an 'all-or-none' process?
During which phase of the cardiac myocyte action potential does the 'plateau' occur, and what ionic events characterize this phase?
During which phase of the cardiac myocyte action potential does the 'plateau' occur, and what ionic events characterize this phase?
What is the primary role of calcium influx during the plateau phase (Phase 2) of the cardiac myocyte action potential?
What is the primary role of calcium influx during the plateau phase (Phase 2) of the cardiac myocyte action potential?
During which phase of the cardiac myocyte action potential does repolarization primarily occur, and what ionic movement is responsible?
During which phase of the cardiac myocyte action potential does repolarization primarily occur, and what ionic movement is responsible?
How do T-tubules contribute to the process of excitation-contraction coupling in cardiac myocytes?
How do T-tubules contribute to the process of excitation-contraction coupling in cardiac myocytes?
What is the function of the sarcoplasmic reticulum (SR) in cardiac myocytes?
What is the function of the sarcoplasmic reticulum (SR) in cardiac myocytes?
What is 'calcium-induced calcium release' in the context of cardiac excitation-contraction coupling?
What is 'calcium-induced calcium release' in the context of cardiac excitation-contraction coupling?
Which proteins are directly responsible for the mechanical contraction of cardiac myocytes?
Which proteins are directly responsible for the mechanical contraction of cardiac myocytes?
What structural feature physically connects adjacent cardiomyocytes, providing mechanical stability during contraction?
What structural feature physically connects adjacent cardiomyocytes, providing mechanical stability during contraction?
How does the coordinated function of cardiomyocytes as a 'functional syncytium' contribute to the heart's overall function?
How does the coordinated function of cardiomyocytes as a 'functional syncytium' contribute to the heart's overall function?
If the voltage-gated calcium channels were blocked during Phase 2 of a cardiac myocyte's action potential, what would be the most likely consequence?
If the voltage-gated calcium channels were blocked during Phase 2 of a cardiac myocyte's action potential, what would be the most likely consequence?
What would happen if the gap junctions between cardiomyocytes were non-functional?
What would happen if the gap junctions between cardiomyocytes were non-functional?
Flashcards
Troponin C
Troponin C
Binds calcium, causing tropomyosin to move and expose actin binding sites.
Tropomyosin
Tropomyosin
Covers actin binding sites, preventing myosin from binding and causing contraction.
Myosin Head
Myosin Head
Forms cross-bridges with actin, powered by ATP, to shorten the muscle during contraction.
Cardiac Excitation-Contraction Coupling
Cardiac Excitation-Contraction Coupling
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Actin
Actin
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Action Potentials
Action Potentials
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Pacemaker Cells
Pacemaker Cells
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Automaticity
Automaticity
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Sinoatrial (SA) Node
Sinoatrial (SA) Node
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Electrical Conduction System
Electrical Conduction System
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Cardiomyocytes
Cardiomyocytes
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Functional Syncytium
Functional Syncytium
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Depolarization
Depolarization
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Membrane Potential
Membrane Potential
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Depolarization Wave
Depolarization Wave
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Phase 4 (Pacemaker)
Phase 4 (Pacemaker)
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HCN Channels
HCN Channels
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Funny Current
Funny Current
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Phase 0 (Pacemaker)
Phase 0 (Pacemaker)
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Calcium Channels (Pacemaker)
Calcium Channels (Pacemaker)
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Phase 3 (Pacemaker)
Phase 3 (Pacemaker)
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Myocytes
Myocytes
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Myocardium
Myocardium
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Phase 4 (Myocyte)
Phase 4 (Myocyte)
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Membrane potential polarity
Membrane potential polarity
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Gap Junctions
Gap Junctions
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Threshold Potential
Threshold Potential
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Phase 0: Depolarization
Phase 0: Depolarization
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All-or-None Process
All-or-None Process
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Phase 1: Initial Repolarization
Phase 1: Initial Repolarization
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Phase 2: Plateau Phase
Phase 2: Plateau Phase
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Sarcoplasmic Reticulum
Sarcoplasmic Reticulum
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Desmosomes
Desmosomes
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T-Tubules
T-Tubules
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Phase 3: Repolarization
Phase 3: Repolarization
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Phase 4: Resting Phase
Phase 4: Resting Phase
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Calcium-induced Calcium Release
Calcium-induced Calcium Release
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Actin and Myosin
Actin and Myosin
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Study Notes
- Action potentials are rapid electrical changes across cell membranes, propagating to adjacent cells, vital for heart communication.
- Pacemaker cells, about 1% of heart cells, initiate heartbeat rhythm by generating action potentials conducted to the other 99% of heart cells.
- Pacemaker cells exhibit automaticity, launching their own action potentials if signals from neighboring cells are absent.
Pacemaker Cell Locations
- Sinoatrial node (SA node) in the right atria sets the pace.
- Internodal tracts connect nodes.
- Atrioventricular (AV) node delays the signal.
- Bundle of His transmits impulses to ventricles.
- Purkinje fibers distribute impulses throughout the ventricles.
Functional Syncytium
- Heart muscle cells or cardiomyocytes receive action potentials slower than pacemaker cells.
- Pacemaker cells act as highways for fast action potential transmission.
- Muscle cells are the slower side roads that help all myocytes contract simultaneously.
- This system enables cells to act as one unit due to mechanical, chemical, and electrical connections.
Action Potential Chemistry
- Action potentials are initiated by depolarization, the opposite of polarization.
- Polarization involves a higher negative charge inside the cell versus outside, defining membrane potential.
- Membrane potential changes are determined by ion movement, specifically which ions move and membrane permeability.
- Depolarization occurs when ions shift, making the membrane potential less negative, potentially positive.
- Depolarization waves in neighboring cells trigger further depolarization, leading to muscle contraction and setting the heart rate.
- Waves that occur once per second result in 60 beats per minute.
Pacemaker Cell Action Potential Phases
- Phase 4: Pacemaker potential phase starts at -65mV.
- HCN channels open when the membrane potential is negative, allowing sodium ions to flow in.
- Inward rush of sodium ions creates the "funny current."
- Sodium influx through HCN channels slowly depolarizes the membrane to -50mV.
- Phase 0: Depolarization phase occurs when the cell reaches -50mV.
- Voltage-gated calcium channels open allowing calcium to flow into the cell.
- Sodium and calcium influx raises the membrane potential past 0mV to +10mV.
- This phase concludes in 0.5 milliseconds
- Phase 3: Repolarization phase as calcium channels start to close at +10mV and potassium channels open.
- Outward positive current from potassium leaving the cell repolarizes the membrane.
- Membrane potential returns to -65 mV, restarting the cycle.
Myocytes
- Myocytes receive signals from pacemaker cells causing them to contract.
- Myocytes make up the myocardium, the muscular middle layer of the heart.
- Myocytes are also called contractile cells because they contract to allow the heart to pump blood.
- Unlike skeletal muscle cells, cardiac myocytes receive signals from pacemaker cells.
Myocyte Action Potential Phases
- Phase 4: Resting phase with membrane potential at -90 mV.
- Gap junctions allow calcium ions to leak in from neighboring cells, raising the membrane potential to -70 mV (threshold potential).
- Phase 0: Depolarization phase commences at the -70mV threshold.
- Voltage-gated sodium channels open, causing a rapid influx of sodium ions.
- Sodium influx raises the membrane potential to +20mV.
- Action potentials follow an all-or-none principle; threshold must be reached for depolarization.
- Phase 1: Initial repolarization happens as the membrane potential rises above -70 mV to +20 mV.
- Sodium channels close, and voltage-gated potassium channels open.
- Potassium ions exit, reducing the membrane potential causing an outward current and a notch on the graph.
- Phase 2: Plateau phase begins when voltage-gated calcium channels open allowing calcium ions to flow into the cell.
- Influx of calcium ions balances potassium outflow, stabilizing the membrane potential.
- Calcium influx triggers myocyte contraction and influences the action potential length and heartbeat.
- Phase 3: Repolarization occurs when calcium channels close, but potassium channels remain open.
- Ion pumps remove calcium ions leading to relaxation.
- Membrane potential returns to -90 mV, restarting the cycle.
Cardiac Excitation-Contraction Coupling
- Cardiac excitation-contraction coupling is relationship between electrical signals and mechanical changes that cause heart muscle contraction.
Cardiomyocyte Structure.
- Cardiomyocytes are branched cells connected by intercalated disks with gap junctions.
- Gap junctions facilitate ion flow between cells, enabling depolarization of neighboring cells.
- Desmosomes physically attach cells, maintaining structural integrity during contraction.
- Transverse tubules (T-tubules) increase surface area and facilitate calcium ion movement deep inside.
- Sarcoplasmic reticulum stores intracellular calcium.
Process
- Depolarization spreads via gap junctions, with calcium ions triggering a threshold in neighboring cells.
- T-tubules enable calcium ions to penetrate deeply into the cell during depolarization.
- Extracellular calcium binds to ryanodine receptors on the sarcoplasmic reticulum triggering calcium-induced calcium release.
- Released calcium activates actin and myosin, essential for muscle contraction.
- Calcium ions bind to troponin C, which moves tropomyosin allowing myosin heads to bind to actin.
- Myosin heads bind to actin, forming cross-bridges and pulling actin and myosin filaments past one another.
- This process requires ATP.
- Calcium ions are removed by ion transporters back into the sarcoplasmic reticulum, extracellular environment, or mitochondria.
- Removal of calcium causes troponin to revert, blocking actin binding sites and preventing further cross-bridges, leading to muscle relaxation.
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Description
Action potentials facilitate rapid electrical changes across heart cell membranes, crucial for intercellular communication. Pacemaker cells, located in areas such as the SA and AV nodes, initiate and regulate heartbeat rhythm. These cells possess automaticity, ensuring continuous heart function.