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BIOSCI 107 Part Two > Muscles: Cardiac Muscle > Flashcards

Muscles: Cardiac Muscle Flashcards

1
Q

Where is cardiac muscle located

A

the heart

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2
Q

Structural features of cardiac muscle cells

A

Striated, Branched cells with 1-3 central nuclei

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3
Q

What connects cardiac muscle cells together

A

intercalated discs

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4
Q

Do muscle cells contract together or separately

A

together

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5
Q

is cardiac muscle voluntary or involuntary

A

involuntary

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6
Q

What does the right side of the heart do

A

it contracts and sends blood to the lungs to become oxygenated

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7
Q

What does the left side of the heart do

A

it receives blood from lungs, contracts and sends blood to the body through the aorta

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8
Q

What are the parts of the heart

A

Right and left atrium and ventricle (4 in total)

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9
Q

What part of the heart has the most muscle

A

The left ventricle

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10
Q

Structural features of ventricular muscle cells

A

they are branched
they contain ~1-3 nuclei
Have many mitochondria for respiration

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11
Q

Where is the T-Tubule located in cardiac vs skeletal muscle

A 
Cardiac = at Z disc
Skeletal = at end of A band/ and I band
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12
Q

Dimensions of ventricular muscle cells

A

100 µm x 30 µm

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13
Q

The two types of junctions in intercalated discs

A

Desmosomes and gap junctions

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14
Q

Function of desmosomes in intercalated discs

A

prevent cells from separating during contraction

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15
Q

Function of gap junctions in intercalated discs

A

allow the AP to be carried from one cell to the next (things like Na+ ions to move AP across cells). Allows for the coordinated contraction of all the myocytes

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16
Q

What does the figure 8 arrangement of cardiac muscles allow the heart to do?

A

Efficiently contract (shorten and narrow) at the same time

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17
Q

Length of Ventricular myocyte AP

A

> 100 ms

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18
Q

What causes the plateau phase in a Ventricular myocyte AP

A

Calcium Voltage gated L channels (causing a large sustained Ca2+ current so the membrane potential stays positive for a period of time). These channels are long acting, long time to open and close

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19
Q

When is the membrane potential of cardiac muscle depolarised

A

Throughout most of the ‘twitch’ (heart beat)

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20
Q

Is an AP longer in cardiac or skeletal muscle

A

Cardiac due to plateau phase

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21
Q

Why does the heart to relax after a contraction before generating a new AP

A

blood need to come into the heart during the absolute refractory period to generate a new AP

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22
Q

3 major stages of an AP in a cardiac muscle cell

A

0 – Rapid depolarisation due to fast voltage gated Na+ channel
2 – Plateau phase due to slow voltage gated Ca2+ channel (L-type Ca2+ channel)
3 – Repolarization due to closing of Ca2+ channels (inward) and opening of K+ (outward) channels

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23
Q

Why is a twitch smaller if generated during relative refractory period of a heart contraction

A

Because the heart hasn’t completely filled with blood due to less relaxation time (there isn’t enough pressure/tension from heart stretching to open aorta)

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24
Q

What is the function of L-type voltage gated calcium channel (LTCC) in excitation contraction coupling in ventricular cells?

A

They can be used to bring calcium into the cell to do the cross bridge cycle

25
Q

What is the function of Ryanodine receptors (RyR) in excitation contraction coupling in ventricular cells?

A

They are a calcium channel in the SR. The trigger for the channel to release Ca from the SR is also Ca

26
Q

What is the function of NCX in excitation contraction coupling in ventricular cells?

A

It is a Na/Ca exchanger

27
Q

What is the function of NKA in excitation contraction coupling in ventricular cells?

A

It is a Na/K ATPase

28
Q

How does cardiac muscle excitation-contraction coupling work

A
  1. Depolarization opens voltage-gated fast Na+ channels in sarcolemma. Reversal of membrane potential from –90 mV to +30 mV (rapid depolarisation)
  2. Depolarization opens slow (L-type) Ca2+ channels in sarcolemma (DHPR)
    Ca2+ influx balanced by a Na+/Ca2+ exchanger. Ca is removed from cell to keep Ca moving in (balanced)
  3. Ca2+ influx triggers opening of Ca2+-sensitive channels in the SR (RyRa), which liberates bursts of Ca2+ (i.e. CA induced CA release) The raised intracellular [Ca2+] allows Ca2+ to bind to troponin, which then switches on the contractile machinery
29
Q

How is Ca2+ removed from cardiac cells

A
  1. SR Ca2+-ATPase (same as skeletal)
  2. Sarcolemmal Na+/Ca2+ exchange
  3. Sarcolemmal Ca2+-ATPase 4. Mitochondrial Ca2+ uniporter.
30
Q

How does relaxation occur in cardiac cells?

A

For relaxation to occur [Ca2+]i must decline, allowing Ca2+ to dissociate from troponin.
This requires Ca2+ transport out of the cytosol

31
Q

Equation for the regulation of cardiac output (CO)

A

Cardiac output = stroke volume x heart rate

CO = SV x HR

32
Q

What is cardiac output (CO)

A

how much blood comes out of the heart is a set period of time normally 5L/min

33
Q

What is a normal cardiac output

A

5L/min

34
Q

What is stroke volume

A

is the volume of blood pumped out of the left ventricle of the heart during each cardiac contraction per min. It reflects the tension developed by the cardiac muscle fibres in one contraction

35
Q

What is a normal stroke volume

A

70ml

36
Q

How to increase stroke volume (3 factors)

A
  1. increased rate of firing (heart rate/HR)
  2. increased stretch of ventricles (length)
  3. certain neurotransmitters (e.g. Noradrenaline)
37
Q

What sets the heart rate

A

is set by the pacemaker cells in the sinoatrial node. The rate can then be modified, especially via the autonomic nerves releasing neurotransmitters

38
Q

What are pacemaker cells

A

Cells in the sinoatrial node that determine the rate of contraction (heart rate)

39
Q

What is the sinoatrial node

A

specialised muscle cells where electrical activity initiates and spreads throughout the heart

40
Q

What is the pacemaker potential

A

This is a slow depolarization to the threshold in pacemaker cells due to If current (mostly Na+ driven) (If = leaky channels) this step is spontaneous

41
Q

Why do pacemaker cells have an unstable resting membrane potential

A

Due to leaky If channels

42
Q

What occurs once the threshold has been reached in pacemaker cells

A

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

43
Q

What causes repolarization in pacemaker cells

A

Repolarization is due to Ca2+ channels inactivating and K+ channels opening.

44
Q

Function of Sympathetic cardiac nerves

A

increase heart rate and force of contraction by releasing noradrenaline

45
Q

Function of the vagus nerve (parasympathetic)

A

Decreases heart rate and releases ACh

46
Q

Why is the intrinsic heart rate higher than the resting heart rate

A

Intrinsic rate is slightly higher than resting rate because at resting your parasympathetic nerve is slowing heart rate

47
Q

What is automaticity

A

Increasing heart rate increases contractile force (stroke volume) due to less time available for Ca2+ to be pumped out of cell

48
Q

What does a higher [Ca] in the heart do

A

More Ca = more myosin can bind to actin (increase heart rate means less time for Ca to be pumped out of the heart, you start from a higher Ca point so when an AP comes there will be more Ca so a stronger contraction)

49
Q

What active tension in cardiac muscle dependent on?

A

the linkage of myosin and actin

50
Q

Why is the resting tension in the heart much higher than skeletal muscle (why is it stiffer - resting/passive tension is higher)?

A

to stop the heart overstretching

51
Q

What does an increased blood volume in the heart do

A

more stretch due to increased blood in heart = more tension = more powerful contraction against it to move blood out of heart to stop over stretching

52
Q

What is Starlings law

A

as the resting ventricular volume is increased the force of the contraction is increased

53
Q

What is the neurotransmitter involved in the neutral control of stroke volume

A

Noradrenaline

54
Q

What does Noradrenaline act on (when controlling stroke volume)

A

β receptors

55
Q

What does the activation of β receptors by Noradrenaline do (when controlling stroke volume)

A

⚈ L-Type channels open resulting in more Ca entering the cell (increasing Ca permeability)
⚈ Ca2+ pump in SR so SR increases its Ca2+ stores (increases store of Ca)

56
Q

What does noradrenaline released by sympathetic nerves do

A

Increases cytosol [Ca] due to increased HR shortening time for extrusion by causing
⚈ increased Ca++ influx (via Ca++ channels) during the action potential (primarily during phase 2),
⚈ increased release of Ca++ by the sarcoplasmic reticulum (due to greater SR uptake)

57
Q

Inotropy

A

ability of the heart to contract and heart rate

58
Q

What does Increased sympathetic stimulation do?

A

results in increased output at any filling pressure due to increase in inotropy

BIOSCI 107 Part Two (17 decks)

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