Lecture 27 - Cardiovascular System: Cardiac Action Potential, Conduction, and Contraction Flashcards
Similarities between cardiac myocytes and skeletal myofibres
They are both striated.
They both have the same organelles, but may be located in different locations (ex. nucleus)
3 differences between cardiac myocytes and skeletal myofibres
Cardiomyocytes usually have only a single, central nucleus and have a branched structure
Reduced in number of T-tubules and sarcoplasmic reticulum in cardiomyocytes
NMJ is absent in cardiac myocytes
How do cardiac myocytes form a functional syncytium?
The syncytium is linked by:
Intercalated discs - physically links the plasma membranes of 2 cells
Gap junctions - allows ions (and thus membrane potential signals) to flow between cells
These linkages mean that myocytes are both physically and electrochemically connected and can act like a large, single unit
Why are cardiac action potentials (APs) prolonged?
They involve the opening of L-type VGCC, which are known for long length of opening and the amount if time it takes for them to get open
T/F? The difference between the contraction cycle between cardiac myocytes and skeletal myofibres is the lack of sliding filaments in cardiac myocytes
False - The contraction cycle in cardiac myocytes involves interactions between sliding filaments, like myofibres. Once Ca2+ is present, the contraction cycles are similar
Describe how Ca2+ plays a role in excitation-contraction coupling in cardiac myocytes
- Some calcium ions enter the cytoplasm from the ECF
- The elevated [Ca2+] triggers the release of much, much more calcium from cellular stores (the SR)
How is the role of Ca2+ different in cardiac myocytes compared to skeletal myofibres?
Ca2+ in cardiac EC coupling has a different relationship between DHPRs and RyRs
In skeletal muscle cells, it plays a role in mechanical coupling, where a change in voltage causes DHPR to pull open the RyR allowing Ca2+ to leave the SR and enter the cytosol. There is no ion flow through DHPR
In cardiac muscle cells, it plays a role in biochemical coupling, where Ca2+ flows through DHPR into cytosol, and the increase in Ca2+ in the cytosol triggers the opening of the RyR, allowing Ca2+ to escape the SR
T/F? Cardiac myocytes cannot produce tetanus
True - due to the duration of the cardiac AP (and its refractory periods). A single AP generates a single contraction (twitch) in both skeletal myofibres and cardiac myocytes, but in cardiac myocytes, a second AP cannot be generated until the twitch is nearly over
How is excitation and contraction of heart chambers synchronized?
Conduction pathways - they are formed from highly modified cardiac myocytes and run through the heart wall. These cells lack myofibrils but are highly excitable and connected by gap junctions
What is the sinoatrial (SA) node?
Where cardiac rhythm begins; it is a pacemaker cell and generate its own rhythm of depolarization and repolarization
What are the 2 parts of the electrical activity of SA node cells?
- Action potential - depolarization is generated by T-type (transient) VGCCs, not VGNCs. Repolarization is generated by VGKCs
- Pacemaker potential - a slow depolarization that automatically restarts after every repolarization
These potentials are calcium-based
What is the “funny channel” and why is it an important component of the pacemaker potential?
The funny channel is a voltage-gated cation channel that only opens when the membrane is hyperpolarized (allowing Na+ to enter the cell)
During the pacemaker potential, a “funny current” (I_f) flows across the cardiac myocyte plasma membrane
Which electrical activity of SA node cells affects the ANS?
Pacemaker potential - changes to this potential affects ANS activity, which causes change in heart rate
Parasympathetic - ACh leads to the opening of additional K+-selective channels. This causes hyperpolarization and slower depolarization (dec. heart rate)
Sympathetic - NE enhances the activation of funny channels. This causes reduced repolarization and more rapid depolarization (inc. heart rate)
Describe the depolarization from the SA node
Depolarization from the SA node spreads through the atrial myocardium and the conduction pathway
SA nodes are electrically coupled to neighbouring cardiac myocytes and to the conducting cells of the internodal fibres, which allow depolarization to rapidly spread across both atria
T/F? The spread of depolarization is faster through the cardiac myocytes than the conduction system
False - it’s faster through the conduction system than the cardiac myocytes because the conduction pathways cells are specialized for rapid electrical conduction. They can conduct APs up to several metres per second