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CST - BIOSCI107 > ET : M - Cardiac Muscle > Flashcards

ET : M - Cardiac Muscle Flashcards

1
Q

How is contraction initiated?

A

Myogenic (involuntary - initiates contractions with nervous input)

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2
Q

What is the conductivity of cardiac muscles?

A

Electrically connected

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3
Q

How are the contractile filaments organised?

A

Into sarcomeres

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4
Q

What is the shape of the SR?

A

Rudimentary

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5
Q

Are cardiac muscles striated?

A

Yes (‘banded’ appearance)

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6
Q

What are cardiac muscles?

A

Forms the bulk of heart mass and its contraction pumps blood

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7
Q

What can’t the force of contraction be modulated by?

A

Recruitment - contraction is all or none

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8
Q

How is the heart structured?

A

A hollow multiple chamber organ, with 2 artrias and 2 ventricles, its volume changes during contraction to pump blood

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9
Q

What is the length and diameter of ventricular cells?

A

100 μm x 30 μm

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10
Q

What are ventricular cells shape?

A

Branched

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11
Q

What do the desmosomes do in ventricular cells?

A

Prevent cells from separating during contraction

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12
Q

What is the function and structure of gap junctions in ventricular cells?

A

Allows action potentials to be carried from one cell to the next, join cells together to form ‘sheets’ that divide and wrap around the ventricles

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13
Q

In ventricular cells, what do intercalated discs allow?

A

For the co-ordinated contraction of all myocytes

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14
Q

How are T-tubules structured in ventricular cells and what is the function of them?

A

Well-developed t-tubular system (at the Z discs), carries excitation into the interior of the cell

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15
Q

Why does the heart have numerous mitochondeia and large amounts of myoglobin?

A

Needs oxygen for oxidative mechanism as the tissue is primarily oxidative (doesn’t want build up of acid (H+))

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16
Q

How many nucleus does ventricular cells have and how does growth occur?

A

Each cell has generally 1 but can have up to 3, growth occurs mainly through hypertrophy with relatively little cell division (after birth)

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17
Q

How are action potentials initiated?

A

In a group of specialised cells in the right atria called the sino-atrial node

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18
Q

Where does the action potential spread?

A

Spreads throughout the atria and then via specialized conducting cells called Purkinje fibres to the ventricles

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19
Q

How long is an action potential?

A

> 100ms

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20
Q

Why is a cardiac action potential quite long lasting?

A

Due to the presence of additional ionic currents that hold the cell membrane potential depolarised throughout most of the twitch (heart beat)

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21
Q

During a ventricular myocyte action potential, what causes fast depolarisation?

A

Na+ influx through fast voltage-gated Na+ channels. A +ve feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase

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22
Q

During a ventricular myocyte action potential, what causes the plateau phase?

A

The Ca2+ influx through slow voltage-gated Ca2+ channels (due to the presence of a large sustained inward Ca2+ current). This keeps the cell depolarized as few K+ channels are open

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23
Q

During the plateau phase of the ventricular myocyte action potential, what does the Ca2+ influx trigger and what is it balanced by?

A

It triggers the release of Ca2+ from the SR by a mechanism called calcium-induced calcium release (CICR). It’s balanced by a large Ca2+ extrusion capacity via a Na+/Ca2+ exchange mechanism

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24
Q

During the plateau phase of the ventricular myocyte action potential, what does the Na+/Ca2+ exchange mechanism produce and lead to?

A

It produces a depolarising current when it extrudes Ca2+, due to the fact that it brings 3 Na+ ions into the cell for each Ca2+ ion it extrudes. This also leads to a prolongation of the action potential

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25
Q

During a ventricular myocyte action potential, what causes repolarisation?

A

The Ca2+ channels inactivation and K+ (outward) channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage

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26
Q

What is highly unlikely to occur during a ventricular myocyte action potential?

A

Summation/tetani of cardiac muscle (long action potential allows twitch to be almost completed before another action potential occurs so while the heart is relaxing, it can pump blood)

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27
Q

In excitation-contraction coupling, what does depolarisation do?

A

Opens voltage-gated fast Na+ channels in the sarcolemma (reversal of membrane potential from -90mV to +30mV).

28
Q

In excitation-contraction coupling, what does depolarisation wave do?

A

Ppens slow (L-type) Ca2+ channels in the sarcolemma (let Ca2+ come into the cell, so this is one source of Ca2+ coming in from outside the cell)

29
Q

In excitation-contraction coupling, what is the Ca2+ influx balanced by?

A

Na+/Ca2+ exchanger

30
Q

In excitation-contraction coupling, what does the Ca2+ influx trigger?

A

Opening of Ca2+ sensitive channels in the SR (RyRa) (as Ca2+ comes in and binds to the RyRa), which liberates bursts of Ca2+ into the cytosol (i.e. CICR)

31
Q

In excitation-contraction coupling, what does the raised Ca2+ intracellular conc. allow?

A

Ca2+ to bind to troponin, which then switches on the contractile machinery (cross-bridge cycle)

32
Q

In excitation-contraction coupling, after contraction, how does relaxation occur?

A

Conc. of Ca2+ must decline, allowing Ca2+ to dissipate from troponin

33
Q

In excitation-contraction coupling, how can Ca2+ be removed?

A
  1. SR Ca2+ ATPase, it gets rid of Ca2+ out of the cytosol, off the troponin and back into the SR
  2. Sarcolemmal Na+/Ca2+ exchange, uses Na+/Ca2+ exchanger (co-transporter), to pump and move Ca2+ out (Na+/K+ ATPase pump generates the gradient for Na+ to move into the cell, down its electrochemical gradient)
34
Q

What triggers the release of Ca2+ from the SR?

A

Ca2+ infux (Ca2+ induced)

35
Q

What is the effect of increasing Ca2+ release?

A

Contraction graded (troponin not usually saturated)

36
Q

How is Cardiac Output (CO) regulated?

A

CO = Stroke Volume (SV) x Heart Rate (HR)

37
Q

What is the heart rate set by and how can the rate be modified?

A

The pacemaker cells in the sinoatrial node (SA node) which is found in the right atria. The rate can then be modified, especially via the autonomic nerves releasing neurotransmitters

38
Q

What is a feature of pacemaker cells?

A

Unstable resting membrane potential

39
Q

In SA + AV node action potential, what is the pacemaker potential?

A

Slow depolarisation, lets Na+ into the cell and the membrane potential drifts up

40
Q

In SA + AV node action potential, what causes depolarisation

A

At threshold, Ca2+ channels open. Explosive Ca2+ influx produces the rising phase of the action potential, sustained by opening of slow Ca2+ channels

41
Q

In SA + AV node action potential, what causes repolarisation?

A

Ca2+ channels inactivating and K+ channels opening

42
Q

What are the sympathethic cardiac nerves?

A

Increase heart rate and force of contraction (e.g. exercise), releases noradrenaline (NA)

43
Q

How does sympathethic cardiac nerves increase the heart rate?

A

Release of NA increases rate of spontaneous depolarisation

44
Q

What are the vagus nerves (parasympathetic)?

A

Decreases heart rate and force of contraction (important for the rest and digest system), release ACh (slow rate of discharge of SA cells)

45
Q

How does vagus nerves (parasympathetic) decrease the heart rate?

A

Release of ACh decreases rate of spontaneous depolarisation and hyperpolarises the resting membrane potential

46
Q

What is the stroke volume?

A

Reflects the tension developed by the cardiac muscle fibres in one contraction

47
Q

How can the stroke volume be increased?

A
  1. Increase the rate of firing (HR - automaticity) (intrinsic)
  2. Increase stretch of ventricles (length) (intrinsic)
  3. Certain neurotransmitters (e.g. NA) to alter rate and Ca2+ handling (direct and rate effects)
48
Q

In automaticity (modulation of force by altering stimulation frequency), increasing the heart rate increases?

A

Contractile force (SV) and therefore, stronger contractions

49
Q

In automaticity, how does Ca2+ affect the heart rate?

A

In cardiac muscle, not all troponin will be saturated so, only some of the binding cells will be exposed. If the Ca2+ conc. gets higher, more of the binding sites become available, more Ca2+ binds with more troponin and more myosin binds onto actin. If heart rate increases, less time between beats for Ca2+ to be pumped out of cell, so tend to start from a higher Ca2+ level in the first place. The longer between beats the more Ca2+ will go back into SR, so Ca2+ level is higher, so when an action potential occurs, have more in the cell and a stronger contraction

50
Q

In the length-tension relationship (modulation of force by muscle length), how is the total tension curve?

A

Very steep, keeps increasing

51
Q

In the length-tension relationship, what is active tension dependent on?

A

Actin and myosin overlap

52
Q

In the length-tension relationship, what don’t we want to happen during passive tension?

A

Heart to expand too much and burst

53
Q

In the length-tension relationship, how is the heart adapted to not overstretch?

A

Has lots of collagen and stiff components so that it can’t be overstretched, which is why passive tension increases the more the heart is stretched

54
Q

In the length-tension relationship, why does the total tension keep increasing?

A

The more the heart is stretched, the more tension and force developed (SV)

55
Q

In the length-tension relationship, what is the result of total tension increasing?

A

The more blood into the heart, the more its stretched, the more powerful the contraction (entirely intrinsic) and blood is pumped out (heart doesn’t get bigger)

56
Q

What is Starlings law of the heart?

A

“As the resting ventricular volume is increased, the force of contraction of the ventricle is increased”

57
Q

In the length-tension relationship, what is there a limit to for cardiac muscles?

A

There is a limit to how big it can get and there is a point where it can’t fill anymore. The higher the atrial pressure, the greater the output (plateau)

58
Q

The heart is innervated by?

A

Autonomic nervous system (i.e. sympathetic and parasympathetic)

59
Q

Sympathetic neurotransmitter (NA) has several effects on the heart via?

A

Second messenger cAMP and protein kinase A

60
Q

What do the sympathetic nerves do in neural control of SV and how?

A

Come down and innervate the ventricles, can adjust the tension that the heart develops. It does this through the NA and acts on the beta receptor (slows heart rate)

61
Q

What does NA upregulate?

A

Ca2+ ATPase. More Ca2+ comes into the cell from outside the cell and SR, increases the pumping ability to get the Ca2+ into the SR. So action potential and twitch shortens as Ca2+ is removed quicker which allows more resting time between the beats

62
Q

How can Ca2+ be removed easier by increasing the pumping ability to get the Ca2+ into the SR?

A

Load Ca2+ in the SR, instead of relying a lot on Ca2+ from extracellular source, have more Ca2+ in the SR so the next beat that comes along, it’s easier to get the Ca2+ out

63
Q

What does NA acts to increase?

A

Increases permeability of Ca2+ coming into the cell and Ca2+ storage capacity inside the cell, so next beat/contraction is going to be bigger and shorter

64
Q

What does a shorter contraction allow?

A

More time for the ventricle to refill between contractions

65
Q

What does NA increases force of contraction via cAMP and protein kinase A?

A
  • Increases the frequency of discharge of SA node cells which increases the frequency of action potentials
  • Increases the amplitude of Ca2+ current, which leads to more Ca2+ entering the cell with each beat
66
Q

What does NA released by sympathetic nerves leads to an increase of and why?

A

Cytosol Ca2+, due to the increased heart rate shortening time for extrusion and via second messengers by:

  • Increasing Ca2+ influx (via Ca2+ channels) during an action potential
  • Increasing the release of Ca2+ by the SR (due to greater SR uptake)
67
Q

What does increased sympathetic stimulation result in?

A

Increased output at any filling pressure due to increase in inotropy (contractability) and heart rate

CST - BIOSCI107 (13 decks)

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