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biosci block 6 & 7 > Lecture 32. Cardiac muscle > Flashcards

Lecture 32. Cardiac muscle Flashcards

1
Q

differences between skeletal and cardiac muscle cells structure

A

Skeletal:
long up to 35 cm
cylindrical
neurogenic( works in response to nerve stimulus)
electrically isolated. Initiating the contraction on one muscle cell does not spread to the other. Need another nerve to innervate the other one
2 t-tubules per sarcomere, at the ends of A band
extensive SR

Cardiac:
shorter ~ 100 um
branched
Myogenic( involuntary)- does not need a nerve signal to work. Generates contraction within itself
electrically couples( AP in one cells spreads to others)
Less t -tubules( 1 per sarcomere) arranged at the Z lines
less SR

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2
Q

Heart anatomy

A

-4 chambers: 2 atria, 2 ventricles

  • Blood comes back into the right atrium from the veins, fills the right ventricle
  • Right ventricle contracts to push the blood to the lungs
  • from the lungs, the blood comes back into the heart through pulmonary veins and fills the left atrium. The left atrium fills the left ventricle.
  • Left ventricle pumps the blood up through the aortic valve and through the aorta to the rest of the body.
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3
Q

Which part of the heart has a thick muscular wall and why?

A

Left ventricle

-contracts to push the blood through the body

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4
Q

How much pressure do right and left ventricles generate?

A

right- ~ 20 mm Mercury

left~ 100 mm Mercury

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5
Q

Structure of ventricular muscle cell

A
  • same sarcomere as in skeletal
  • t-tubules line up with the Z disc. Half as many t-tubules in the heart muscle
  • SR is less associated with the t-tubules, not as extensive-> not as reliant on Ca2+ from SR
  • Not so much Ca2+, it does not bind to every troponin-> the amount of contraction can be regulated by the amount of Ca2+ bound to troponin.
  • Intercalated discs join muscle cells together
  • size: 100 um x 30 um
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6
Q

What junctions are in intercalated discs?

A
  • desmosomes

- gap junctions

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7
Q

what is the role of desmosomes in the heart muscle?

A

Desmosomes prevent cells from

separating during contraction

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8
Q

what is the role of gap junctions in the heart muscle?

A

allow the action potentials to be carried from one cell to the next
• Allows for the coordinated contraction of all the myocytes
(unlike skeletal muscle where fibres are recruited via the motor nerves)

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9
Q

How do ventricles contract?

A
  • inwards and outwards

- important to pump the blood up

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10
Q

Why is it important for the heart to relax?

A

during relaxation, it fills up with blood

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11
Q

How is the heart protected from tetanic contractions?

A

-long AP > 100 ms
-important not how fast it depolarizes by the plateau phase
-Has plateau phase due to presence of a large sustained
Ca2+ current (ICaL).
-After depolarization K+ channels open together with the Ca2+ channels
-The twitch is almost over before the membrane gets to the hyperpolarized state
-One twitch is finished as AP is finished-> impossible to get an overlap of twitches

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12
Q

L type Ca2+ channel

A

-extra Ca2+ channel in the heart myocyte
-V-gated
-slow to open and close-> takes longer for Ca2+ to come into the cell
-

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13
Q

Comparison of AP length and contraction in skeletal vs cardiac muscle

A
  • skeletal muscle AP is over before the contraction is generated, allowing for another AP to be generated and overlap of contractions to happen
  • in cardiac muscle almost impossible to have a tetanic contraction AP and contraction happen at the same time
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14
Q

3 major stages of AP in cardiac muscle cell

A

0 – Rapid depolarization due to fast voltage-gated Na+ channel
2 – V-gated Na+ channels close. V-gated K+ channels are starting to open. Plateau phase due to slow voltage-gated Ca2+ channel (L-type Ca2+ channel)
3 – Repolaristation due to closing of Ca2+ channels and opening of K+ (outward)
channels

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15
Q

contraction and relaxation time

A

contraction 1/3 sec

relaxation 2/3 sec

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16
Q

why are early premature contractions in the heart small?

A

the heart did not have enough time to fill

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17
Q

Contraction duration and refractory period

A

-the earliest another contraction can start is when the AP is in the refractory period, but it will be small

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18
Q

effect of exercise on muscle contraction

A

every phase speeds up-> not change in ratio of them to each other

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19
Q

how is calcium getting out of the cardiac muscle cell?

A

through Na+/Ca2+ exchangers on the t-tubules. Na+ goes in, Ca2+ goes out

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20
Q

Where are Ca2+ channels RyR located in the cardiac muscle?

A

ryanodine receptors( Ca2+ channels) are located in the SR

Unlike in skeletal muscle, where the receptors are on t-tubules

21
Q

What do ryanodine receptors in cardiac muscle respond to?

A

Ca2+ and NOT voltage

Ligand-gated channels.

22
Q

how is Ca2+ released in cardiac muscle cell?

A

Need some Ca2+ to come in ( through L-type Calcium channels) and bind to the ryanodine receptors to open the Ca2+ channels and the Ca2+ to flow out of SR

->Ca2+ induced Ca2+ release

23
Q

What channels are present on t-tubules and SR in cardiac muscle?

A

On t-tubule:

LTCC = L-type voltage gated calcium channel (ICaL)
NCX = Sodium/Calcium exchanger
NKA = Sodium/potassium ATPase
V-gated Na+ channels
On SR:
RyR = ryanodine receptor (Calcium channel in sarcoplasmic reticulum)

24
Q

what is dihydropyridine receptor (DHPR)?

A

another name for L-type Ca2+ receptors

25
Q

excitation-contraction coupling process

A
  • Depolarization opens voltage-gated fast Na+ channels in the sarcolemma. Reversal of membrane potential from –90 mV to +30 mV
  • Depolarization wave opens slow (L-type) Ca2+ channels in the sarcolemma (DHPR)

• Ca2+ influx balanced by a Na+/Ca2+
exchanger

• Ca2+ influx triggers the opening of Ca2+-sensitive channels in the SR (RyRa),
which liberates bursts of Ca2+ (i.e. calcium-induced calcium release)

• The raised intracellular Ca2+ concentration allows Ca2+ to bind to troponin,
which then switches on the contractile machinery

26
Q

How is Ca2+ removed from the cytoplasm after contraction?

A
  • most of it is pumped back into the SR through Ca2+ ATPase( SRCa2+ ATPase)
  • Need to get Ca2+ out of the cell- Na+/Ca2+ exchanger- can go in both directions
  • Can also go out of the cell through other Ca2+ ATPases
  • or goes into mitochondria- Ca2+ uniport
27
Q

Calcium spark

A

fluorescent agent reacts to calcium

produced by the Ca2+ coming out of the SR-> contraction

28
Q

differenced in AP in cardiac and skeletal muscle

A

In cardiac muscle:

  • longer AP
  • regulated by Ca2+ influx. Ca2+ induced Ca2+ release
  • rudimentary SR
  • contraction graded by Ca2+ -troponin not usually saturated
  • recruitment of more fibers does not happen
29
Q

cardiac output

A

the amount of blood pumped out of the body in a set time( 1 min)
-average 5 L per min( for 70 kg male)

CO= SVx HR

30
Q

exercise affect on Cardiac Output

A

both SV and HR increase

31
Q

how is heart rate set?

A

by a specialized muscle in the synal atrial node

-generate AP.

32
Q

AP generation in the heart

A

-generates in the cell in the SA node, spreads across atria, reaches the AV node, spreads around the ventricles

33
Q

where are cells with Pacemaker potential found?

A

SA and AV node

34
Q

cells with pacemaker potential

A
  • act as the nerve
  • trigger AP
  • the rate at which these cells beat determines the heart rate
  • do not have stable RMP
  • spontaneously depolarises by itself
35
Q

steps of AP generation by the pacemaker cells

A

Pacemaker potential:
This slow depolarization is Due to If current (mostly Na+ driven). NA+ leaks into the cells

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

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

36
Q

Nerves that regulate the heart rate(adjust)

A

-vagus nerve(parasympathetic)- only affects heart rate
acts on SA and AV node
Slows the HR
releases Ach

-Sympathetic cardiac nerves
increase HR and force of contraction
Innervate the ventricles
releases NA

37
Q

What neurotransmitter is released by parasympathetic nerves?

A

Ach

decreases HR

38
Q

What neurotransmitter is released by sympathetic nerves?

A

Noradrenaline

39
Q

Neural control of the HR

A
  • Vagal nerve hyperpolarises the RMP-> slows HR

- Sympathetic depolarises the RMP, and the rate of depolarization is higher

40
Q

‘automaticity’

A

• Increasing heart rate increases contractile force (stroke
volume)
- due to less time available for Ca2+ to be pumped out of the cell. In between beats- Ca2+ is pumped out. As the time between beats decreases- less Ca2+ leaves, and more Ca2+ accumulates.More Ca2+ goes into the SR rather than out of the cell-> more Ca2+ is released each time.

1HZ= 60 beats/min

41
Q

Length tension relationship in the heart

A

-more stretched the heart is- the stronger the contraction

• Increased stretch (filling=preload) results in more force developed (stroke volume)

42
Q

what is the general pressure of right atrium?

A

2 mm Hg

43
Q

Starlings law

A

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

TOTALLY INTRINSIC- NO NERVES REQUIRED

44
Q

How do nerves control stroke volume?

A
  • Noradrenaline interacts with a beta-receptor coupled with a G-protein, which increases cAMP -> phosphorylation-> upregulation of Ca2+ channels in the sarcolemma and SR-> more influx of Ca2+ for each contraction
  • Also upregulates the SRCa2+ pump, which takes Ca2+ back into SR
  • Changes troponin affinity to Ca2+-easier to bind and release

Net result- bigger/shorter contraction

45
Q

Noradrenaline vs adrenaline

A

Noradrenaline- neurotransmitter released from the sympathetic nerves
Adrenaline- the hormone in the blood, released in response to sympathetic stimulation of the adrenal gland

BOTH INCREASE THE FORCE OF CONTRACTION IN THE HEART

46
Q

why is it important during exercise to have shorter contractions?

A
  • even with increased HR and Cardiac output and increased force of contraction of the heart, the contraction is shorter so that the heart can still be filled
47
Q

Neural control of stroke volume

A

Noradrenaline released by sympathetic nerves leads to increased cytosol calcium
due to increased HR shortening time for extrusion. And via second messengers :
- by increasing Ca++ influx (via Ca++ channels) during the action potential (primarily during phase 2),
- by increasing the release of Ca++ by the sarcoplasmic reticulum (due to greater SR uptake)

Increased sympathetic stimulation results in increased output at any filling pressure due to an increase in Stroke Volume AND Heart rate

48
Q

In what ways can SV and HR be increased?

A
  • Increased HR
  • Stretch the muscle( length-tension relationship)- increased SV- INTRINSIC
  • Via nerves and neurotransmitter noradrenaline( sympathetic)- increased HR and SV
49
Q

main differences between skeletal and cardiac muscle

A

In cardiac muscle:

  • AP generated within the muscle at the SA node
  • Myogenic initiation of contraction-involuntary
  • Electrically coupled conductivity
  • AP longer~ 100 ms
  • Ca2+ release from SR is trigerred directly by Ca2+

biosci block 6 & 7 (8 decks)

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