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Muscles Flashcards

1
Q

What is the structure of terminal ends of motor neurones?

A
  1. At the end of a motor neurone, the axon becomes unmyelinated and separates into multiple branches (1-2 μm).
  2. At the end of each branch, there is a plate-like structure called a bouton which forms the pre-synaptic terminal between the motor neurone and one muscle fibre.
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2
Q

What is the name given to all muscle fibres innervated by one motor neurone?

A

Motor unit

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3
Q

What is the structure of a neuromuscular junction (NMJ)?

A
  • On the post-synaptic membrane (sarclemma), there’s inward invaginations every 1-2 μm called junctional folds.
  • Above each junctional fold is a thickening in the bouton called the active zone.
  • Within each active zone are rows of thousands of neurotransmitter vesicles.
  • These vesicles fuse with the pre-synaptic membrane within these zones and are released into synaptic cleft by exocytosis.
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4
Q

What is the basal lamina?

A
  • In the synaptic cleft is a network of proteins (e.g. collagen, laminin) and mucopolysaccharides.
  • This forms the glue that ‘sticks’ the end plate to the sarcolemma.
  • This also contains high concentration of AChE to terminate synaptic transmission.
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5
Q

What is the width of the synaptic cleft?

A

~50 nm

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6
Q

What is the sequence of events that occur at NMJ during synaptic transmission?

A
  1. AP arrives at bouton (post-synaptic terminal) and depolarises it.
  2. Depolarisation causes voltage-gated Ca2+ channels to open, which causes an influx of Ca2+ down electrochemical gradient and an increase in intracellular [Ca2+].
  3. Increase in intracellular [Ca2+] increases the probability of ACh vesicles fusing with the pre-synaptic membrane in the active zones.
  4. Vesicles fuse with pre-synaptic membrane and ACh is released into the synaptic cleft by exocytosis.
  5. ACh diffuses across the synaptic cleft and binds to AChR, opening associated ion channels and causing influx of Na+ which depolarises the sarcolemma (EPP).
  6. Depolarisation causes opening of voltage-gated Na+ channels (in the folds), which causes AP to occur.
  7. ACh is broken down by AChE in the synaptic cleft into acetate and chlorine that diffuse back into the bouton where they are re-synthesised into ACh.
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7
Q

What is the enzyme that synthesises ACh?

A

Choline acetyltransferase (from choline and Acetyl-CoA)

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8
Q

What is the synaptic delay and what is responsible for it?

A
  • Delay between the time of action potential arrival at the pre-synaptic terminal and the time an EPP occurs in post-synaptic terminal.
  • The time taken for Ca2+ to cause vesicle fusion is thought to be mainly responsible for this delay.
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9
Q

What is the relationship between [Ca2+] and probability of vesicle fusion?

A

Probability is proportional to [Ca2+]^4

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10
Q

What is the structure of the AChR?

A
  • N1 ACh receptor
  • Ligand-gated ion channel
  • 5 subunits (2α, β, γ, δ)
  • ACh binding sites located on the α subunits?
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11
Q

What are the advantages of having 2 ACh binding sites?

A
  • Opening probability proportional to [ACh]^2
  • Prevents channel from opening when ACh is very low but dramatically increases opening probability of channels when [ACh] is high.
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12
Q

What are the kinematics of the AChR?

A
  • 2 ACh molecules need to bind to both sites on the AChR before it opens.
  • Over-stimulation causes AChR to inactivate, preventing depletion of trans-membrane ionic gradients.
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13
Q

What is the resting potential of muscles?

A

~-90 mV

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14
Q

What is the reversal potential of AChRs?

A

~0 mV

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15
Q

What is the function of curare in research?

A

Blocks AChRs and allows EPSPs to be observed.

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16
Q

What is the function of physostigmine in research?

A

Allows the amount of ACh released on stimulation of pre-synaptic terminal to be measured.

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17
Q

what is the pathophysiology of myasthemia gravis?

A
  • Autoimmune disease.
  • Caused by autoimmune attacks on AChRs, reducing their numbers and preventing stimulation of skeletal muscles.
  • Causes weakness and paralysis of skeletal muscles.
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18
Q

What was concluded from the observation of MEPPs?

A

ACh was stored and released from the pre-synaptic terminal in packets (quanta). This suggested that ACh was stored in vesicles.

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19
Q

What are the characteristics of ACh release during EPPs?

A
  • When multiple EPPs were measured in low extenal [Ca2+], a pattern was observed.
  • About each multiple of 0.4 mV was a normally distributed curve called a ‘bin’. Each bin represented a fixed number of ACh molecules released and the normal distribution of the bins represented the variations in ACh content of each vesicle.
  • The peaks of each bin formed a poisson distribution. This showed that the probability of each vesicle fusing with the presynaptic membrane is independent of each other, but is increased with an increase in intracellular [Ca2+].
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20
Q

What are the proteins involved in release of ACh by exocytosis?

A

Vesicle:
- Synaptobrevin (v-SNARE): Binds to t-SNAREs on the pre-synaptic membrane.
- Synaptotagmin: Ca2+ sensor.
Pre-synaptic membrane:
- Syntaxin (v-SNARE): Binds to snaptobrevin.
- SNAP-25 (v-SNARE): Binds to synaptobrevin.
- n-SEC-1: Inhibits syntaxin.
Recycling:
- α-SNAP
- NSF (ATPase)

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21
Q

What is the general structure of muscles?

A

Muscle → Fascicles → Muscle fibres → Myofibrils → Sarcomeres

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22
Q

What are the features of a skeletal muscle fibre?

A
  • Sarcolemma: Plasma membrane
  • Sarcoplasm: Cytoplasm
  • Transverse (T-) tubules: Involved in EC coupling
  • Sarcoplasmic reticulum: Specialised endoplasmic reticulum acting as Ca2+ store
  • Nuclei: Muscle fibres are multinucleate
  • Mitochondria: Produces ATP for cross-bridge cycling
  • Myofibrils: Contractile mechanism
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23
Q

What is the diameter of a muscle fibre?

A

50-100 μm

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24
Q

What is the significance of titin in skeletal muscles?

A
  • Titin is a protein believed to attach myosin to the Z-disc.
  • It has a role in generation passive tension in muscles.
  • It also has vital role in determining the length-tension relationship of muscle via the lattice rearrangement model.
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25
Q

What additional molecules are abundant in muscles?

A
  • Myoglobin

- Phosphocreatinine

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26
Q

What is the structure of actin filaments?

A
  • Backbone of actin filament made from 2 strands of F-actin wrapped around each other in an α helical arrangement.
  • Each F-actin filament is a polymer of G-actin molecules (like strand of beads).
  • Tropomyosin is a filamentous molecule that are packed into the grooves between the F-actin molecules. Each tropomyosin spans around 7 G-actin molecules.
  • Tropomyosin blocks the binding sites of myosin on F-actin.
  • Troponin complexes are also bound at regular intervals.
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27
Q

What is the structure of troponin?

A
  • Troponin consists of 3 subunits.
  • Troponin C (TnC): Binidng site for Ca2+ ions.
  • Troponin T (TnT): Binding site of troponin for tropomyosin.
  • Troponin I (TnI): Supposedly binds to F-actin.
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28
Q

What is the structure of myosin?

A
  • Myosin filaments are bundles of myosin II molecules.
  • Each myosin II molecule consists of 2 myosin heavy chains wrapped around each other with 2 light chains attached to the head groups of each.
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29
Q

What is the structure of myosin heavy chains?

A
  • Rod: Rod regions of each heavy chain wrapped around each other to form helical structure holding the heavy chains together.
  • Hinge: Part of the heavy chain that moves during cross-bridge cycling.
  • Head: Contains actin binding site as well as ATPase domain that hydrolyses ATP.
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30
Q

What are the types of myosin light chains?

A
  • Alkali: Helps stabilise structure of head group.

- Regulatory: Regulates activity of ATPase domain in head group by undergoing phosphorylation/dephosphorylation.

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31
Q

What is the structure of troponin C?

A

Contains 2 high affinity Ca2+ binding sites always occupied by Ca2+/Mg2+ and 2 low affinity binding sites that are occupied by Ca2+ when intracellular [Ca2+] is high.

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32
Q

What is the process of myofibril activation when intracellular [Ca2+] is high?

A
  1. Ca2+ binds to low affinity binding sites on troponin C.
  2. Conformational change occurs whereby troponin I is moved, allowing movement of tropomyosin.
  3. Troponin T moves tropomyosin deeper into the groove between F-actin molecules, thus exposing the myosin binding site on F-actin and allowing cross-bridge cycling to take place.
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33
Q

What are the steps of cross-bridge cycling?

A
  1. Binding of ATP to myosin head causes it to detach from its binding site on F-action.
  2. Hydrolysis of ATP to ADP and Pi moves myosin head to a 45∘ angle in the ‘cocked’ state.
  3. New cross-bridge forms between the myosin head group and a new binding site on actin further down from the previous site.
  4. Release of Pi causes the power stroke to occur. The myosin head bends back to its relaxed state at and angle of 90∘, carrying the actin filament with it. This pulls the actin filament towards the M-line of the sarcomere.
  5. ADP is released from the head group and another ATP binds, allowing the cycle to repeat.
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34
Q

What is the cause of rigor mortis?

A

Absence of ATP means that the myosin head groups are stuck to the actin, causing the muscle to enter a rigid state.

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35
Q

What are the sources of ATP for the duration of exercise?

A
  1. Initially, the small amount of ATP present in the muscles is able to last for 1-2 seconds (8 twitches) from beginning of exercise.
  2. Phosphocreatinine phosphorylates ADP to ATP. The ATP generated from this process lasts another 4 seconds (~100 twitches).
  3. Glycogen in the muscle is then used up in oxidative phosphorylation. This lasts another 10 seconds.
  4. When glycogen is used up, the liver begins breaking down fats to fatty acids for use by the muscles.
  5. If fatty acid supply runs out, the muscles begin breaking down protein for energy.
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36
Q

Why do bicycles need gears?

A
  • From the velocity-power graph of muscles, it can be seen that maximum power is achieved at a certain velocity of contraction.
  • Gears ensure that regardless of the velocity of the bicycle, peddling velocity is matched to that which produces the maximum power output by the muscles.
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37
Q

What are the different types of muscle fibres?

A
  • Type I (red) fibres: Aerobic, slow twitch fibres that rely on aerobic respiration for ATP production.
  • Type II (white) fibres: Anaerobic, fast twitch fibres that rely on anaerobic respiration for ATP production.
38
Q

What is the purpose of T-tubules?

A
  • To carry APs from the sarcolemma into the sarcoplasm.
  • This is because muscle fibres are so large that APs at the sarcolemma cause little current to flow in the sarcoplasm.
  • Increases the surface area of sarcolemma and amplifies the effects of the EPP (greater surface area, more energy released due to greater capacitance).
39
Q

What is the structure of a triad in skeletal muscles?

A
  • Each triad consists of a T-tubule in contact with flattened structures at the borders of 2 separate SR called terminal cisternae.
  • Triads are located at the A-band/I-band junction.
40
Q

What are the different types of ion channels in muscle plasma membrane?

A
  • Voltage gated Na+ channels: Causes AP.
  • K+ channels (several types).
  • Cl- channels: Stabilises resting potential of muscle.
  • Ca2+ channels: CICR in cardiac muscles.
41
Q

What are the types of K+ channels present in muscle plasma membranes?

A
  1. Delayed outward rectifying K+ channels (like those in neurones for repolarisation)
  2. Further delayed outward rectifying K+ channels
  3. Inward rectifying K+ channels
42
Q

What are the functions of inward rectifying K+ channels in muscles?

A
  • Reduces outward repolarising K+ currents.

- Minimises loss of intracellular K+ after repeated stimulation.

43
Q

What are the functions of differences between muscle and neurone APs?

A
  • Muscles APs are longer in duration. This could be due to the inward rectifying K+ channels reducing repolarising K+ current.
  • Slower conduction velocity due to large surface area of muscle membrane, which increases capacitance and thus time constant, decreasing velocity.
44
Q

What is the sequence of events in EC coupling?

A
  1. EPP causes AP to be generated in the sarcolemma.
  2. APs propagate across sarcolemma and into the T-tubules.
  3. Depolarisation due to AP causes conformational changes in ‘voltage sensors’ in the T-tubule membrane. These are L-type Ca2+ channels.
  4. At the triad junctions, the Ca2+ channels are in physical contact with Ca2+-release channels (ryanodine receptors) in the terminal cisternae membranes of the SR via the cytoplasmic foot processes on the release channels.
  5. Conformational changes in the voltage sensor causes conformational changes in the release channels that result in their opening via mechanical activation.
  6. Ca2+ released from the SR through these channels induce neighbouring release channels to open via CICR. This positive feedback event results in rapid increase in intracellular [Ca2+] in the muscle, causing contraction.
45
Q

What is malignant hyperthermia caused by?

A

Mutations in ryanodine receptor result in inability to close, which results in uncontrollable Ca2+ release from SR and muscle spasms.

46
Q

How is contraction ended?

A
  • Ca2+ is extruded from the sarcoplasm through the sarcolemma (via NCXs and PCMAs).
  • Ca2+ is re-uptaken into the SR by sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA) in exchange for H+.
  • 2 Ca2+ molecules pumped into SR for every 1 ATP hydrolysed.
47
Q

What is the role of calsequestrin?

A
  • Calsequestin is a Ca2+ binding protein.
  • It acts as a buffer for [Ca2+] in the SR.
  • Since SERCA activity is inhibited by high SR [Ca2+}, calsequestrin sequesters Ca2+ and reduces SR [Ca2+].
  • This allows for Ca2+ to be loaded into the SR without much change in SR [Ca2+], thus allowing continuous Ca2+ loading into the SR.
  • This increases the amount of Ca2+ that can be re-uptaken by the SR, allowing cytoplasmic [Ca2+] to be returned to sub-contraction levels.
48
Q

How many Ca2+ molecules can 1 calsequestrin bind to?

A

45

49
Q

What are the mechanisms of controlling contraction strength?

A
  • Temporal summation (tetany): Creates strong, smooth contractions.
  • Spatial summation: Variation in the number/size of motor units allow finer control over contraction strength than is allowed by tetany.
50
Q

What are the structural features of intercalated discs?

A
  • Gap junctions: Contains connexon channels that link cytoplasms of adjacent myocytes together. Allows currents to pass directly from one cell to the next and thus cardiac muscles act as electrical syncytium.
  • Gap desmosomes: Adhesion proteins that mechanically link cardiac myocytes together.
51
Q

What are the types of cardiac myocytes present in cardiac muscle?

A
  • Sinu-atrial node
  • Atrial myocytes
  • Purkinje (conducting) fibres
  • Atrioventricular node
  • Ventricular myocytes
52
Q

What are the functions of sinu-atrial node cells?

A
  • Pacemaker for whole heart
  • Myogenic
  • Directly causes atrial systole and indirectly causes ventricular systole
53
Q

What are the functions of atrial myocytes?

A
  • Conduction

- Atrial systole

54
Q

What are the functions of purkinje fibres?

A
  • Conduction
  • Refractoriness (excitability gap)
  • Pacemaking (when 3rd degree heart block occurs)
55
Q

What are the the functions of atrioventricular node cells?

A
  • Directly causes ventricular systole

- Pacemaking (when SAN damaged

56
Q

What are the functions of ventricular muscle?

A
  • Conduction

- Ventricular systole§

57
Q

What are the features of a typical cardiac myocyte AP?

A
  • 0: Rapid depolarisation due to opening of voltage-gated Na+ channels once the membrane has depolarised above threshold.
  • 1: Inactivation of Na+ channels and the slow activation of Ca2+ channels means that there is a brief period of repolarisation where the outward K+ channel dominates.
  • 2: Opening of Ca2+ channels counteract the outward K+ current and holds membrane at depolarised potential. This is the plateau phase.
  • 3: The membrane repolarises as more slow-activating K+ channels open and the outward current dominates the inward current.
  • 4: Membrane returns to resting potential of around -90mV (electrical diastole).
58
Q

What is the significance of the inward Ca2+ current during AP in cardiac myocytes?

A
  • Responsible for the plateau phase of the AP.
  • Responsible for CICR and is essential in bringing about cardiac muscle contraction.
  • Inward rectifying K+ channels decrease the outward K+ current and so reduces the inward Ca2+ current, which aids in maintaining Ca2+ gradient.
59
Q

What is the mechanism of self-excitation in pacemaker cells?

A
  1. At rest, there is an inward depolarising current from pacemaker cells. This is called the funny current (I_f).
  2. The I_f depolarises the membrane to beyond threshold, which causes voltage-gated Na+ channels to open.
  3. This results in depolarisation and the disappearance of I_f.
  4. Once the membrane repolarises to resting potential, I_f reappears to depolarise cell to threshold and retrigger APs.
60
Q

What is the cause of I_f?

A
  • The main contributor towards I_f are hyperpolarisation-activated cyclic nucleotide-gated channels (HCNs). these are non-selective cation channels.
  • Other contributors towards I_f are Na+ and Ca2+ channels also open at rest.
61
Q

What is the sequence of events during a cardiac contraction?

A
  1. Depolarisation of the SAN causes excitation of surrounding atrial myocytes.
  2. Wave of excitation spreads across atria and causes atrial systole.
  3. Band of insulating tissue between the atria and ventricles prevents wave of excitation from spreading to the ventricles.
  4. Wave of excitation passes through AV node much slower than the atria (due to presence of less gap junctions between nodal cells).
  5. Wave is conducted down the interventricular septum through atrioventricular bundle (bundle of His), which splits into the left and right bundle branches, allowing wave to be carried into the left and right ventricles respectively.
  6. Wave of excitation carried by purkinje fibres 2/3 up ventricles and then spreads the remainder through the myocytes themselves.
62
Q

What is the role of the conduction delay through the AV node during cardiac contractions?

A

Conduction delay ensures that ventricular systole occurs after atrial systole, which allows maximum filling of ventricles before systole.

63
Q

What is the purpose of ensuring that wave of depolarsation travels from apex upwards?

A

Ensures that ventricles contract from apex upwards, pushing blood up and out of the vessels located at the top of the heart.

64
Q

What is responsible for prolonged refractory periods in cardiac myocytes?

A

Longer APs as a result of plateau phase ensures that the absolute refractory period is longer.

65
Q

What is the significance of excitability gap?

A
  1. Ensures that no temporal summation occurs and that there is no tetany in cardiac muscles.
  2. Ensures that the wave of excitation only travels in one direction and no re-entry arrhythmias arise.
66
Q

What is overall heartrate dictated by?

A

The fastest group of pacemaker cells

67
Q

What is the discharge rate of respective nodes in the heart?

A

SAN: 60-80/min
AVN: 40-60/min
Purkinje fibres: 30-40/min

68
Q

What are the dimensions of a cardiac myocyte?

A
  • Diameter: 10μm

- Length: 200μm

69
Q

What is the sequence of events in EC coupling in cardiac muscles?

A
  1. AP generated in SAN myogenically and propagates along the plasma membrane of cardiac myocytes.
  2. AP propagates down T-tubules extending into the cytoplasm of myocytes.
  3. AP causes voltage-gated L-type Ca2+ channels in T-tubule membrane to, which causes influx of Ca2+ ions into cytoplasm at the diads between T-tubules and SRs.
  4. Increased intracellular Ca2+ causes CICR from SR, which causes positive feedback system that further increases intracellular [Ca2+].
  5. Ca2+ binds to TnC and causes conformational change that allows cross-bridge cycling to begin.
70
Q

What are the differences between EC in skeletal muscles compared to cardiac muscles?

A
  1. T-tubule system found at A/I junction in skeletal muscles while they are found at the Z-line in cardiac muscles.
  2. In skeletal muscles, EC coupling depends on mechanical coupling between L-type Ca2+ channels and ryanodine receptors while in cardiac muscle, EC coupling is achieved through CICR and Ca2+ influx through L-type Ca2+ channels.
  3. In skeletal muscles, there is a very small influx of Ca2+ from sarcolemma Ca2+ channels that don’t contribute significantly to rise in Ca2+ for contraction. In cardiac muscles however, influx of Ca2+ is large and does contribute (due to 5x larger T-tubule diameter).
  4. Amount of Ca2+ released from SR of skeletal muscles always enough to cause contraction, but not for cardiac muscles. Instead, extracellular Ca2+ makes significant contribution.
  5. In skeletal muscles, grading of contraction strength is controlled by temporal (tetanus) and spatial summation. In cardiac muscle however, these are not possible and separate mechanisms are used.
71
Q

What evidence is there to support the fact that skeletal EC coupling is mechanical and cardiac muscle is not?

A
  • In skeletal muscle, rise in intracellular [Ca2+] occurs after AP.
  • In cardiac muscle, rise in intracellular [Ca2+] occurs simultaneously with AP.
72
Q

What is the consequence of external Ca2+ having bigger role in cardiac muscle EC coupling?

A
  • Strength of cardiac muscle contraction can be altered by varying amount of Ca2+ influx (by varying Ca2+ permeability).
  • This is not possible with skeletal muscles.
73
Q

Why is spatial and temporal summation not possible in cardiac muscles?

A
  • Spatial summation: Because of the excitability gap and extended absolute refractory period of cardiac myocytes.
  • Temporal summation: Because the cardiac myocytes are connected to each other by gap junction, making them electrical syncytium, so individual myocytes can’t be stimulated.
74
Q

How is intracellular Ca2+ extruded?

A
  • SERCAs, back into the SR.
  • NCXs and PCMAs extrude extracellular Ca2+ entering myocytes during contraction to avoid build-up of Ca2+ within the myocytes.
75
Q

What is the significance of Ca2+ extrusion by NCXs?

A
  • NCXs are electrogenic (1 Ca2+ out, 3Na+ in).
  • The more a myocyte contracts, the greater the activity of NCXs, the more the myocyte becomes depolarised.
  • This has the effect of causing cardiac arrhythmias in patients suffering from tachycardia.
76
Q

What are the ways that cardiac myocyte contractility is controlled?

A
  • Passive: Frank-Starling mechanism

- Active: Hormonal and neural control

77
Q

What are the effects of vagal (parasympathetic) stimulation of the heart?

A
  • ↓ Heart rate

- ↓ Contractility

78
Q

What are the mechanisms behind parasympathetic stimulation?

A
  • Vagus nerve releases ACh, which acts on the SAN and increases resting K+ permeability. This hyperpolarises nodal cells and increases time take for I_f to depolarise cell beyond threshold.
  • ACh also causes cGMP-dependent phosphorylation of L-type Ca2+ channels, which decreases influx of external Ca2+ during contraction, decreasing contractility.
  • Vagus nerves only innervate the SAN.
79
Q

What are the effects of sympathetic stimulation of the heart?

A
  • ↑ Heart rate

- ↑ Contractility

80
Q

What are the mechanisms behind sympathetic stimulation?

A
  • Sympathetic nerves release NAd, which acts on the SAN and increases resting Ca2+ and Na+ permeability. This increases I_f and results in time for nodal cells to depolarise beyond threshold to decrease.
  • NAd also causes cAMP-dependent phosphorylation of L-type Ca2+ channels, which increases contractility.
  • Sympathetic nerves innervate the whole of the myocardium.
81
Q

What are the characteristics of the P-wave?

A
  • ≤ 0.12s wide and ≤ 0.3mV high.

- Wider/higher suggests atrial hypertrophy

82
Q

What are the characteristics of the P-Q interval?

A
  • Between 0.12-0.24s wide.
  • If too short, suggests short-circuitry and presence of alternate conduction pathway.
  • If too long, suggests 1st degree heart block.
83
Q

What are the characteristics of QRS complex?

A
  • ≤ 0.12s wide.
  • If too long, suggests bundle-branch block.
  • Sum of peaks should be ≤3.5mV.
  • If too large, suggests ventricular hypertrophy.
84
Q

What are the characteristics of QT interval?

A
  • ≤0.45s wide.

- If too wide, suggests long QT syndrome.

85
Q

What are the ways in which smooth muscle contraction is stimulated?

A
  1. ↑ [Ca2+]i → Ca2+ binds to and activates calmodulin (Ca2+-CaM) → Calmodulin binds to caldesmon (bound to actin and prevents cross-bridge cycling) → Caldesmon dissociates and cross bridge cycling begins.
  2. ↑ DAG (through PLC pathway) → ↑ PKC activity → ↑ Caldesmon phosphorylation → Caldesmon dissociates and cross bridge cycling begins.
  3. ↑ [Ca2+]i → Ca2+ binds to myosin light chain → ↑ myosin head ATPase activity → ↑ Rate of cross-bridge cycling.
  4. Ca2+-CaM complex binds to and activates myosin light chain kinase (MLCK) → Phosphorylation of myosin light chains → ↑ Myosin head ATPase activity → ↑ Rate of cross-bridge cycling.
  5. Calmodulin binds to calponin (also binds to and inhibits actin), causing its dissociation and allowing cross-bridge formation.
86
Q

How is smooth muscle contraction stimulated?

A
  1. ↑ [Ca2+]i

2. Pharmaco-mechanical coupling

87
Q

How is contraction stimulated in smooth muscle cells by APs?

A
  1. Nervous stimulation causes opening of Ca2+ channels and Ca2+ influx causing AP. AP causes opening of more Ca2+ channels and causes greater influx.
  2. Initial influx of Ca2+ from nervous stimulation causes CICR from ER in smooth muscles.
88
Q

How is contraction stimulated in smooth muscles by pharmaco-mechanical coupling?

A
  1. Hormones that stimulate PKC pathway causes production of IP3, which opens Ca2+ channels in ER and causes efflux of Ca2+, increasing intracellular [Ca2+] and causing contraction.
  2. PKC pathway also stimulates DAG production, which binds to caldesmon and directly stimulates contraction.
89
Q

How are latch-bridges formed?

A
  • Dephosphorylation of myosin light chain by myosin phosphotase while head group still attached to actin via cross-bridge locks head group to cross-bridge.
  • Allows sustained smooth muscle contraction with minimal energy expenditure, making smooth muscles 300 times more efficient than skeletal muscle.
90
Q

What are the types of smooth muscle APs?

A
  1. Spike AP
  2. Plateau AP
  3. Slow wave AP
91
Q

What is the Bowditch effect?

A
  • Contractility increases with heart rate.
  • Increased heart rate caused by more frequent cardiac myocyte depolarisation.
  • Greater Ca2+ influx into the cardiac myocyte.
  • More Ca2+ loaded into SR, causing more Ca2+ release in subsequent contraction, leading to greater contractility.

Homeostasis (15 decks)

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