Exam #2: Cardiac Excitation-Contraction Coupling Flashcards
What is the sequence of electrical events in the heart?
SA node → AV node → Bundle of His → Bundle branches (L and R) → Purkinje fibers
What is the purpose of the AV nodal delay?
Ensures atrial contraction precedes ventricular contraction, allowing for complete ventricular filling between beats
What is the only step of the pathway that conducts from the atria to ventricles?
AV node → Bundle of His
What type of cells use a fast action potential?
Conductile cells and Contractile cells
What type of cells use a slow action potential?
Pacemaker cells (AV and SA node cells)
What type of ion drives fast action potentials?
Na+
What type of ion drives slow action potentials?
Ca2+
What ion/channel does the ANS act on?
Na+ funny channels
With fast depolarization, what event is responsible for the rapid depolarization (upstroke)? What type of channel?
Na+ rapidly flowing into cell (ordinary voltage-gated channels)
With fast depolarization, what event is responsible for the plateau phase? What type of channel?
Ca2+ slowly flowing into cell (L-type channels)
With fast depolarization, what event is responsible for the rapid repolarization? What type of channel?
K+ rapidly flowing out of cell (ordinary voltage-gated channels)
With fast depolarization, what event is responsible for the return to resting membrane potential? What type of channel?
K+ slowly flowing out of cell (leaky channels)
What is the purpose of the plateau phase?
It increases the duration of the action potential and allows time for the contraction to occur (time for plateau phase = time for full contraction then relaxation)
- Avoid cardiac tetany
Why is the RMP for cardiac muscle -90 mV instead of the -70 mV?
K+ permeability is even higher in cardiac cells (MANY:1 when comparing K+:Na+)
With slow depolarization, what event is responsible for the slow depolarization? What type of channel?
- Na+ slowly flowing into cell (funny channels)
- Ca2+ slowly flowing into cell (L-type channels)
What is another name for the slow depolarization phase in slow APs?
Pacemaker potential because this phase sets the HR
With slow depolarization, what event is responsible for the rapid depolarization?
Ca2+ flowing into cell
With slow depolarization, what event is responsible for the rapid repolarization?
K+ flowing out of cell
What type of muscle is cardiac muscle similar to in terms of excitation-contraction coupling? How is it different?
Cardiac muscle is very similar to skeletal muscle EXCEPT:
- Cardiac cells also receive Ca2+ from the ECF via L-type channels
What are the three ways by which intracellular Ca2+ is decreased?
- SERCA (most significant)
- Na+/Ca2+ exchanger - uses Na+/K+ ATPase
- Sarcolemmal Ca2+ ATPase
What is the relationship between tension/contraction, sarcomere length and volume?
They are all directly related:
- If sarcomere length increases, tension/contraction increases and volume will also increase
How does the SNS affect contractility/inotropy?
Positive contractility/inotropy effect
How does the PNS affect contractility/inotropy?
Negative contractility/inotropy effect
What type of receptors are utilized by the SNS with relation to contractility/inotropy? What type of protein are they coupled with and what is their action?
SNS = B1 receptors
- Coupled to Gs proteins and AC, which activates cAMP and PKA
Which two types of proteins are phosphorylated by cAMP during SNS stimulation? What is the action of each in increasing contractility?
- Sarcolemmal Ca2+ channel: increases Ca2+ release from SR
- Phospholamban: increases Ca2+ uptake and storage into SR (pumps it back into SR)
What is the general affect that phospholamban activity has on heart rate
Contraction is briefer aka faster relaxation (increased HR)
What type of receptors are utilized by the PNS with relation to contractility/inotropy? What type of protein are they coupled with? WHAT part of the heart do they specifically act on?
PNS = muscarinic receptors
- Coupled to Gi proteins
Decrease contractility in ATRIA
With PNS and muscarinic receptors, when ACh is released, what are the two actions it takes to decrease contractility?
OVERALL, what is the general affect of these two actions combined?
- ACh decreases flow of Ca2+ into the cell during plateau phase (less Ca2+ available for contraction)
- ACh increases K+ current which shortens the duration of the AP and indirectly (further) decreases flow of Ca2+ into the cell during plateau phase
OVERALL, ACh decreases the amount of Ca2+ entering atrial cells during an AP AND decreases the amount of Ca2+ being released from the SR
What is the mechanism behind Na+-K+ ATPase blockers? How does this happen, and what affect does this have?
Inhibit Na+/K+ ATPase
- No K+ flows in and no Na+ flows out through Na+/K+ ATPase
- Na+ accumulates inside cell
- Na+ is pumped out of cell via Na+/Ca2+ exchanger, so Ca2+ is pumped into the cell
- Increased Ca2+ inside cell = increased contractility
What is the mechanism behind calcium-channel blockers (3)?
- Decreased contractility
- Decreased HR
- Decreased conduction velocity
What is the mechanism behind B-Agonists blockers?
- Increase cAMP production
- Increase protein phosphorylation
- Increase Ca2+ influx = Increased contractility
