Cardiac Physiology: Excitation-Contraction Coupling

Questions and Answers

What is the primary function of intercalated disks in cardiomyocytes?

To connect cardiomyocytes to skeletal muscles

To allow ions to flow between cardiomyocytes (correct)

To increase the surface area of cardiomyocytes

To store intracellular calcium

Which process directly follows the binding of calcium to ryanodine receptors?

Release of calcium ions into the extracellular space

Activation of actin and myosin

Expansion of the sarcoplasmic reticulum

Calcium-induced calcium release (correct)

What role do transverse tubules (T-tubules) play in cardiomyocytes?

They increase the surface area allowing better ion exchange (correct)

They serve as attachment points for desmosomes

They initiate depolarization in the cardiomyocyte

They store calcium ions for muscle contraction

What happens to tropomyosin when calcium binds to troponin C?

It slides off the actin filament, exposing binding sites Signup and view all the answers

How are calcium ions removed from cardiomyocytes after contraction?

They are actively transported using ATP Signup and view all the answers

What structure allows cardiomyocytes to stay physically attached to one another?

Desmosomes Signup and view all the answers

What is the main role of the sarcoplasmic reticulum in cardiomyocytes?

To store and release calcium ions Signup and view all the answers

During the contraction of cardiomyocytes, what is the effect of the power stroke performed by myosin heads?

It shortens the actin and myosin filaments Signup and view all the answers

Study Notes

Cardiac Excitation-Contraction Coupling

Cardiac excitation-contraction coupling connects electrical signals to mechanical contractions in cardiomyocytes.
Contraction is initiated by electrical depolarization and calcium ion movement.

Cardiomyocyte Structure

Cardiomyocytes feature branched structures enhancing connectivity.
Intercalated disks on cardiomyocytes ensure adjacent cell communication.
Gap junctions within intercalated disks allow ion flow, enabling rapid electrical propagation.
This connectivity forms a functional syncytium, enhancing collective cardiac contraction.
Desmosomes maintain physical connections between adjacent cardiomyocytes.
T-tubules, extensions of the cell membrane, increase surface area for ion exchange.
The sarcoplasmic reticulum serves as a calcium storage site, crucial for muscle contraction.

Calcium-Induced Calcium Release

A depolarization wave triggers calcium ion influx via gap junctions.
Threshold membrane potential leads to the opening of sodium channels.
T-tubules facilitate deep penetration of calcium ions into the cardiomyocyte.
Calcium binds to ryanodine receptors on the sarcoplasmic reticulum, releasing additional calcium (calcium-induced calcium release).
Released calcium activates actin and myosin, initiating muscle contraction.

Actin/Myosin Interaction

Calcium binds to troponin C, altering tropomyosin's position on actin filaments.
Tropomyosin's movement reveals binding sites on actin for myosin heads.
Myosin heads form cross-bridges with actin, enabling contraction through a power stroke mechanism.
Contraction involves multiple cycles of binding, sliding, and reattachment of myosin to actin.
Myosin heads act like oars, facilitating muscle shortening as they pull actin and myosin past each other.

Calcium Removal

Calcium ions are actively transported back into the sarcoplasmic reticulum or out of the cell, utilizing ATP and concentration gradients.
Some calcium is also directed towards mitochondria for energy metabolism.
Absence of calcium restores troponin to its original shape, blocking actin binding sites.
This prevents further cross-bridge formation, leading to muscle relaxation.

Description

This quiz explores the intricate mechanisms of cardiac excitation-contraction coupling, highlighting how electrical signals translate to mechanical contractions in cardiomyocytes. It covers cardiomyocyte structure, calcium dynamics, and the role of intercalated disks. Test your knowledge on the essential components of cardiac muscle physiology!