Excitable cells Flashcards

(99 cards)

1
Q

What are the three major types of structural cell in the cardiovascular system?

A
  • Cardiac myocytes
  • Vascular smooth muscle
  • Vascular endothelium
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2
Q

What are cardiac myocytes?

A

‘Myo’ = muscle
‘cyte’ = cell
Cardiac muscles = type fo striated muscle

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3
Q

What are the two types of cardiac myocyte?

A
  • Basic myocyte
  • Modified myocyte
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4
Q

What is a basic myocyte?

A

Do the mechanical contractile work and don’t contract until stimulated by an impulse.

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5
Q

What is a modified myocyte?

A

Form the basis of the conduction system. Some such cells are able to initiate an electrical impulse.

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6
Q

Describe the anatomy of a cardiac myocyte

A
  • Single nucleus
  • Length may not run the entire length of the muscle
  • Each myocyte may be branched
  • Cardiac myocyte cells exist in a branching network called a syncytium (unit) which results results from a fusion of cells
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7
Q

How are myocytes attached within a syncytium?

A
  • End-to-end by a stepped junction
  • These junctions are called intercalated discs
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8
Q

What two types of junction exist within the intercalated disk?

A
  • Gap junctions
  • Desmosomes
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9
Q

What are gap junctions?

A
  • Myocyte membranes are very close
  • Spanning the gap is a tube called a connexon which opens into the cytoplasm in the cells either side
  • Offer a low resistance pathway to ion flow from cell to cell
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10
Q

What are desmosome junctions?

A
  • Serve to rivet the cell together
  • Glycoprotein that spans the space between adjacent myocyte membranes.
  • Desmosomes give the myocyte its tensile strength
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11
Q

Key - What specifically about cardiac myocytes allows the heart to contract as a unit?

A
  • If one cardiac myocyte is electrically stimulated, the rapid cell-to-cell conduction ensures that the electrical impulse will travel to all the interconnected myocytes almost simultaneously
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12
Q

Myocytes reviewed microscopically

A
  • Each myocyte is composed of myofibrils
  • Myofibrils contain myofilaments
  • When myocytes are viewed microscopically, distinct repeating lines and bands can be seen, each represents different myofilament compounds
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13
Q

What are Z-lines in cardiac conduction cells?

A

The lateral boundaries of the sacromere
They are critical structural and signalling components that anchor the actin filaments and titin.

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14
Q

What is a sarcomere?

A

A basic contractile unit, the segment between two z-lines
Each sarcomere contains thin and thick filaments which account for 50% of the cell volume
Sarcomeres are joined end to end and aligned in register across the myocyte (giving stripy appearance)

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15
Q

Key - What does the length of the sarcomere determine?

A

The force of the myocyte contraction

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16
Q

What are thick filaments comprised of?

A

Myosin

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17
Q

What do thin filaments contain?

A

Actin and other associated proteins

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18
Q

What causes sarcomere shortening?

A

Chemical interactions between actin and myosin filaments

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19
Q

What connects a myosin filament to the z-lines?

A
  • Titin - a large filamentous protein
  • This helps keep the myosin in the centre of the sarcomere
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20
Q

Key - What is the benefit of titin having elastic properties?

A

Plays an important role in the passive mechanical properties of the heart.

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21
Q

What does each myosin molecule have?

A
  • 2 heads
  • The site of myosin adenosine triphosphatase
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22
Q

What is an enzyme?

A
  • Proteins which speed up the rate of a biological reaction without being used in the reaction themselves
  • Work by binding with one substance and converting it into another substance
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23
Q

What does myosin ATPase react with?

A

ATP in a chemical reaction with water

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24
Q

What is ATP required for?

A
  • Building cross bridges between actin and myosin filaments
  • This is necessary for contraction
  • The molecules interact with a binding site on actin
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25
What is within each myosin head?
Regulatory subunits that can alter the myosin ATPase activity
26
What surrounds each thick myosin filament?
A hexagonal arrangement of thin filaments comprised of actin, tropomyosin and troponin
27
What is actin?
Chain of repeating globular units forming two helical strands. Between the strands are rod-shaped proteins called tropomyosin Each tropomyosin molecule is associated with seven actin molecules Attached to the tropomyosin at regular intervals is a troponin regulatory complex
28
What is the troponin regulatory complex?
Made up of; - Troponin-T (TN-T) which binds to tropomyosin - Troponin-C (TN-C) which binds to calcium ions - Troponin-I (TN-I) which binds to actin and acts as an inhibitor This whole complex holds the tropomyosin in position stopping the myosin heads binding with actin.
29
Key - What is used in a blood test to confirm an infarction has occurred?
TN-I and TN-T in the circulation When myocytes die (MI) TN-I and TN-T are released into the circulation
30
How is the relationship between stimulation of the cells by an impulse and mechanical contraction of the heart described?
Excitation-contraction coupling
31
What membrane surrounds a bundle of myofibrils?
Sarcolemnal (surface) membrane
32
Describe T-tubules
- Deep invaginations in the sarcolemnal membrane called transverse tubules (T-tubules) that run deep into the cell interior. - Exist opposite the z-lines - Job = transmit electrical stimulus rapidly to the interior of the cell and activate myofibrils almost simultaneously.
33
What do T-tubules permit?
Ion exchanges to occur between the outside and deep within the inside of the myocyte cell.
34
What is the sarcoplasmic reticulum?
Extensive branching tubular network inside the cell in close proximity to T-tubules
35
Why is the sarcoplasmic reticulum of major importance?
- It contains a store of Ca++ ions - These are partially released into the sarcoplasm on electrical activation of the cell.
36
The release of what activates the contraction mechanism?
Ca++
37
What brings about contraction of the heart?
The shortening of each sarcomere
38
How are sarcomeres shortened?
- By a 'sliding filament' mechanism - The thin filaments slide into the spaces between the thick filaments
39
How are cross bridges formed?
- Filaments are propelled past each other by the repeated making and breaking of biochemical bonds called 'crossbridges' - Crossbridges are actually the myosin heads which protrude from the side of the thick filament
40
What is the role of tropomyosin rods when the cell is at rest?
Prevent myosin heads from binding with actin
41
After cell depolarisation, what happens to calcium?
Ca binds to some of the TN-C of the troponin complex.
42
What happens after calcium binds to some of the TN-C of the troponin complex?
- Causes a structural change in the troponin-tropomyosin complex which results in exposure of the myosin binding sites on actin.
43
What happens when myosin binding sites on actin are exposed?
Myosin head can now bind to the actin forming a crossbridge.
44
How are force and movement generated? (myosin head)
- A change in the angle of the myosin head advances the filament by 5-10nm
45
What happens following a myosin head advancing?
- The head disengages itself and process repeats itself at new actin site further along the filament - This process occurs with numerous sites along the filament - The thick filament essentially 'rows' itself between the thin filaments using the myosin heads as oars.
46
What determines the number of cross-bridges formed?
The amount of calcium released
47
What causes a submaximal contraction?
- Ca++ concentration released by the sarcoplasmic reticulum in cardiac myocytes is only sufficient to activate a fraction of potential crossbridge sites
48
Key - what activates more crossbridges?
Anything that increases the amount of intracellular calcium e.g. adrenaline - This causes the heart to beat more forcefully.
49
Key - the force of contraction is proportional to what?
The number of crossbridges formed and therefore to sarcoplasmic Ca++ concentration.
50
Where do myosin heads get the energy they need for 'rowing'?
- ATP - ATP binds to an ATPase active site on the myosin head after the head has disengaged from actin - ATP broken into ADP and inorganic phosphate - Energy released - The energy propels the myosin head back into a firing angle ready to form a new cross-bridge - The stroke power of the myosin head is powered by the energy of the ATP hydrolysis
51
What does every crossbridge formation/detachment require?
An ATP molecule
52
How is ATP manufactured?
- In the mitochondria of the cell - Process requiring oxygen
53
Where are myocytes fused?
Syncytium
54
How are syncytium joined?
By intercalated disks which have gap junctions essential for rapid conduction
55
What are myocytes composed of?
Bundles of myofibrils
56
What are myofibrils composed of?
Myofilaments
57
What does microscopic viewing of myofibrils show?
Distinct bands corresponding to myofilament components
58
What are z-lines?
The distance between 2 is the sarcomere which is the basic contractile unit of the myocyte
59
What does the length of the sarcomere determine?
The force of contraction
60
Name three myofilaments
- actin - myosin - titin
61
What is myosin?
- Thick filament - Has myosin molecule heads that can bind wit sites on actin
62
Where are ATPase sites?
On myosin heads
63
What is actin?
- Thin filament, lies either side of the thick filament - Globular helical double string
64
Where are tropomyosin rods?
Within actin
65
What prevents myosin from binding with actin?
Troponin complex attached to tropomyosin rods at specific intervals
66
What does calcium released from sarcoplasmic reticulum bind with?
TN-C on troponin complex
67
What happens when calcium binds with TN-C on troponin complex?
- Alters structure of complex so that myosin head can bind with actin. - Crossbridges are formed.
68
What determines the force of contraction?
The number of crossbridges
69
What causes the sarcomere to shorten (contract)?
Crossbridge formation/breaking 'rows' the thick filament past the thin filament
70
Describe the relationship between excitation and contraction
- The pacemaker-conduction system of the heart is made up of modified muscle tissue (not nervous tissue) - Electrical discharge is conducted from cell to cell by ionic currents flowing through local circuits. - When electrical discharge reaches the muscle fibres they are excited and fire an action potential. - The action potential initiates a rise in intracellular calcium ion concentration. - This activates the contractile mechanism of the cell.
71
Importance of electrical impulses
- Vital to all cardiac functions - Trigger cardiac muscle contraction - Organise the sequence of muscle contraction during each cardiac cycle - Pattern and timing of impulses determines the heart rhythm.
72
What is electrical activation?
The process of depolarisation and its spread over the myocardium (myocyte cells)
73
How is electrical potential measured?
-mV - Quoted as a comparison of the voltage inside of the cell with the outside
74
What causes electrical potential?
- Concentrations of positively and negatively charged ions either side of the membrane - The permeability of the membrane to these ions - Permeability of the cell membrane to different ions changes with transmembrane potential.
75
What ions are most important in determining transmembrane potential?
- Sodium (Na+) - Calcium (Ca++) - Potassium (K+) - Chloride (Cl-)
76
Which ion is the most important in determining the resting membrane potential?
K+
77
Describe concentration of K+ inside and outside of a cell
In a cardiac myocyte, K+ is high inside the cell and low outside of the cell
78
Describe cell membrane permeability to K+
High permeability
79
Explain what happens to charge when K+ ions leave the cell
Negatively charged intracellular ions like inorganic phosphates and proteins cannot accompany the K+ out of the cell because the membrane is not permeable to them. - Therefore when K ions leave the cell, there is a tiny separation of charge
80
Describe the potassium equilibrium potential
If intracellular potential reached -94mV, the negative electrical attraction to K ions into the cell would balance with the tendency for K to move out of the cell down its concentration gradient - So there would be no movement of K ions - The electrical potential at which this would happen is the potassium equilibrium potential - This can be calculated using Nernst's equation
81
Describe the creation of non-equilibrium
While K is at equilibrium, there is a small inward current of positive Na+ ions. The amount of Na+ is small because the membrane is not very permeable to Na+ at such negative potentials as a result, resting potential remains slightly more positive than the K equilibrium potential.
82
Key point - Summarise relationship between ions and membrane potential
- Continuous trickle of K out of the cell because potential does not reach the equilibrium for K+ - Outward current of ions is balanced by an equal and opposite inward current of ions so that - The resting membrane remains stable at -90mV despite continuous slow exchange of K+ for Na+ - A cell is said to be polarised when resting transmembrane potential is -90mV
83
Key - Describe phase 0 of purkinje myocyte action potential
- The slope of the voltage spike in phase 0 represents speed of depolarisation and so determines how soon the next cell will depolarise. - Determines the speed at which the impulse propagates across the heart. - If we do something which changes the slope of phase 0, we can change the speed of conduction of cardiac tissue
84
What is the process of repolarisation?
Process of resetting the ion channels
85
Describe phase 1
- Repolarisation begins - Transient outflow of K+ from the cell. - This ionic current inactivates itself rapidly
86
Describe phase 2
- The 'plateau phase' - Interupts repolarisation because: Calcium channels in the membrane allow calcium into the cell This long-lasting current prolongs the refractory and gives duration to the action potential
87
Describe phase 3
- Brings repolarisation to an end - Calcium channels inactivated - K+ ions flow out of cell unopposed - This rectifies the balance of ions - K+ channels become inactive as it becomes more dominant within the cell
88
Describe phase 4
- The resting phase between two action potentials - In terms of ionic currents it is relatively static - No significant net movement of ions across the cell membrane during this period
89
Summarise repolarisation
- Repolarisation returns the action potential to the resting transmembrane potential - It takes time to do this - The time that it takes to do this is called the refractory period of cardiac tissue
90
What is the ERP?
- During phase 0,1,2 and part of 3 the cell is refractory (unexcitable) - This means new action potentials cannot be started (because the Na+ gates remain closed - The period is called the effective refractory period which serves as a protective mechanism in the heart - it limits the frequency of action potentials and therefore contraction - This means the heart has time to fill and eject blood before the next contraction
91
Describe pacemaker cells
- No true resting potential - Generate regular spontaneous action potentials - This ability = automaticity - Many sodium gates are inactivated in pacemaker cells. - Depolarisation occurs because of relatively slow inward calcium currents which gradually increase potential to threshold value -40mV
92
What happens in pacemaker cells once threshold of -40mV is met?
- More calcium channels open - Influx of calcium is not rapid like the Na+ in ordinary myocytes - Therefore depolarisation occurs more slowly in pacemaker cells - Depolarisation eventually causes potassium gates to open - There is an outward current of K+ ions returning the cell to its original state - This happens fairly slowly
93
Why does the SA node drive heart rate?
- It initiates action potentials more quickly than other pacemaker cells in the conduction system - This means that myocytes are depolarised from by the impulse from the SA node before any of the other part of the conduction system generates an action potential.
94
What happens if the SA node fails or becomes depressed?
- Another part of the conduction system may initiate action potentials. - This will generate a heartbeat from an ectopic focus
95
Key - What controls the changes in the rate of action potential generation of the SA node?
The nerves that act upon it
96
Key - How does vagal tone affect heart rate?
High vagal tone lowers heart rate and blood pressure, as the vagus nerve is the primary driver of the parasympathetic "rest and digest" response. Conversely, low vagal tone is associated with a higher resting heart rate and can be a sign of stress, as the sympathetic nervous system is more dominant. This relationship is why increased vagal activity leads to a slower, more variable heartbeat, which is a key indicator of cardiovascular health.
97
How does vagal tone effect the SA node?
Vagal tone decreases the heart rate by slowing the firing rate of the sinoatrial (SA) node. At rest, a high "vagal tone" (increased parasympathetic activity) is dominant and lowers the heart rate from its intrinsic rate of \(100-110\) beats/min to a typical resting rate of \(60-80\) beats/min. Vagal stimulation slows the SA node's firing rate by reducing the speed of diastolic depolarization. 
98
What do the shape of action potential graphs show?
- Conduction velocity - Refractoriness - Automaticity of cardiac tissue
99
Explain the relationship between the ECG and action potentials
The ECG is a sum of the action potentials over time