Cardiac Muscle Flashcards
1
Q
Cardiac Muscle
A
- made up of cardiac myocytes
- interconnected by intercalated disks
- has striations
- less abundant, but larger T-tubules than skeletal muscle and runs perpendicular and parallel to muscle fibres
- smaller amounts of SR bc cardiac muscle requires entry of extracellular Ca2+
- abundance of mitochondria
- oxidative metabolism
2
Q
Intercalated Disks
A
- Desmosomes: link mechanically
2. Gap Junctions: link them electrically
3
Q
Autorhythmic Cells
A
- pacemakers
- generate action potentials spontaneously
- the depolarization begins in the Sinoatrial node
- non-contracting myocardial cells
- smaller and contain few contractile fibres
4
Q
Electrical Conduction in Myocardial Cells
A
- autorhythmic cells spontaneously fire AP’s
- depolarization of autorhythmic cells spread rapidly to adjacent contractile cells through gap junctions
5
Q
Cardiac Conduction Process
A
- SA Node
- Internodal Pathways
- AV Node
- Av Bundle
- Bundle Branches
- Purkinje Fibres
6
Q
HCN Channels
A
- only in auto rhythmic cells
- Hyperpolarization-activated cyclic nucleotide-gated channels
- responsible for funny current)
7
Q
AP’s in Autorhythmic Myocardial Cells
A
- HCN channels open (start at -60mV to -40mV)
- some Ca2+ channels (T-type) open, HCN channels close
- lots of Ca2+ channels (L-type) open
- Ca2+ channels close, K+ channels open
- K+ channels close
- repeat
8
Q
AP’s in Contractile Myocardial Cells
A
- ions entered from AP are transferred to adj. cells through gap junctions
1. Resting Potential
2. Na+ channels open (causing Na+ action potential spike)
3. Na+ channels close
4. Ca2+ channels open (L-type channels); fast K+ channels close leads to sustained depolarization
5. Ca2+ channels close; slow k+ channels open (hyperpolarization)
6. Resting potential
9
Q
Why have a Long Action Potential in Cardiac Muscle
A
- prevents summation of contraction
10
Q
Excitation-Contraction Coupling in Cardiac Muscle
A
- DHP receptors are NOT mechanically coupled to RyR
- Ca2+ entry is necessary for contraction
11
Q
Excitation-Contraction Coupling Process in Cardiac Muscle
A
- action potential enters from adjacent cell
- voltage-gated Ca2+ channels open. Ca2+ enters cell
- Ca2+ induces Ca2+ release through RyR
- local release causes Ca2+ spark
- summed Ca2+ sparks create a Ca2+ signal
- Ca2+ ions bind to troponin to initiate contraction
12
Q
Cross Bridge Cycling
A
- increase in [Ca2+]I triggers contraction by removing the inhibition of cross bridge cycling
- tropomyosin shifts
- Ca2+ binds to troponin
- release of Pi strengthens bond btwn actin and myosin
13
Q
Relaxation of Cardiac Muscle
A
- reuptake into the SR is primary mechanism
- removal of Ca2+ to extracellular space is more important in cardiac muscle
14
Q
Relaxation Process of Cardiac Muscle
A
- current spreads through gap junctions to contractile cell
- AP travel along plasma membrane and T-tubules
- Ca2+ channels open in plasma membrane and SR
- Ca2+ induces Ca2+ release from SR
- Ca2+ binds to troponin, exposing myosin-binding sites
- cross bridge cycle begins
- Ca2+ is actively transported back into the SR and ECF
- Tropomyosin blocks myosin-binding sites (muscle fibre relaxes)
15
Q
Phospholamban
A
- regulates the SERCA pump in cardiac muscle
- crucial regulator of cardiac contractility
- dephosphorylated state PLN inhibits SERCA
- phosphorylated: Ca2+-pump inhibition removed, enhancing relaxation rates and contractility
- rate and amount of Ca2+ uptake is increased, causing quicker relaxation and a larger store of Ca2+ for subsequent contractions
16
Q
Enhancing Contractile Force in Cardiac Muscle
A
- Increase in intracellular Ca2+ in cardiac myocytes enhances contractile force
- Length tension relationship
- cardiac muscle generates a greater force when slightly stretched
17
Q
Increase in Intracellular Ca2+ in Cardiac Myocytes
A
- cardiac muscle is capable of graded single twitch contractions
- if cytosolic Ca2+ is low some actin remains covered by tropomyosin
- increased: additional troponin complexes activated and increased cross bridge formation leading to increased force of contraction
18
Q
Neuronal Inputs in the Heart
A
- innervated by the autonomic nervous system
- sympathetic increases heart rate/conduction (auto rhythmic and contractile)
- parasympathetic decreases heart rate/conduction (autorhythmic)
19
Q
Sympathetic Modulation of Contraction
A
- Phosphorylation of Ca2+ channels causes the calcium channels to remain open longer during action potentials
- Phosphorylation of RyR enhances sensitivity to Ca2+, increasing release of Ca2+ from SR
- increases rate of myosin ATPase
- Phosphorylation of SERCA (PLN) increases the speed of Ca2+ re-uptake which increase Ca2+ storage
20
Q
Sympathetic Activity of Heart
A
- results in a more rapid and forceful contraction
- increase tension in shorter amount of time
21
Q
Cardiac Length Tension Relationship
A
- a slightly stretch sarcomere increases the Ca2+ sensitivity of the myofilaments
- a stretched sarcomere has a decreased diameter which may reduce the distance that Ca2+ needs to diffuse increasing probability of cross-bridge cycling
- as slightly stretched sarcomere puts additional tension on stress-activated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release
22
Q
Heart Rate is under Tonic Control
A
- auto rhythmic cells can be modulated by sympathetic and parasympathetic neurons
- sympathetic: increases
- parasympathetic: decreases
- resting heart rate: 70-72 bpm when parasympathetic is dominant
23
Q
Parasympathetic Modulating Pacemaker Activity
A
- Parasympathetic neurons containing ACh mainly innervate the SA and AV node influencing autorhythmic myocardial cells, decreasing frequency of heart rate/AP’s
- ACh acts on muscarinic cholinergic receptors opening K+ channels and closing T-type Ca2+ channels and HCN channels
- these mechanisms act at the AV node to decrease conduction velocity
24
Q
Decrease Conduction Velocity
A
- block HCN channels: slower depolarization requires more time to reach threshold
- K+ (GIRK) channels: starting at a more negative value, requires more time
- T-type Ca2+ channels: slow channels, so takes more time
25
Q
Sympathetic Modulation of Pacemaker Activity
A
- Beta1 adrenergic receptors can be activated by NE released from sympathetic neurons or Epinephrine from the adrenal medulla
- increased Na+ conductance through HCN channels and Ca2+ through T-type causes: cell to reach threshold more rapidly and a decreased level of repolarization
