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PBL SEM 2 > PBL 4 - control of cardiac contractility > Flashcards

PBL 4 - control of cardiac contractility Flashcards

1
Q

what are the contractile/working cells of the heart?

A

cardiomyocytes

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2
Q

what is the role of cardiomyocytes?

A

to contract in unison in order to provide effective pump action to ensure adequate blood perfusion of the organs and tissues

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3
Q

what is the approx size of cardiomyocytes?

A

approx 100um x 20um — make up the bulk of the volume of the heart but constitute to only 30-40% of the total cell number

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4
Q

how to cardiomyocytes attach to each other?

A

attach end-to-end via intercalated discs

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5
Q

label this diagram of gap junctions

A
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6
Q

what do gap junctions do?

A

transmit ionic currents from one cell to the next

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7
Q

what is each gap junction made up of?

A

6 connexin subunits which form a hollow tube known as the connexon

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8
Q

the connexon tube spans the 2-4nm intercellular gap, enabling the myocardium to what?

A

to act as an electrically continuous sheet and all the myocytes to be activated simultaneously

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9
Q

what are desmosomes?

A
  • ‘glue’ cells together
  • specialized adhesive protein complexes that localize to intercellular junctions and are responsible for maintaining the mechanical integrity of tissues
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10
Q

describe the structure of desmosomes

A
  • glycoproteins called cadherins span the 25nm gap between the cell membranes
  • desmin forms the intermediate filaments
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11
Q

label this diagram

A
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12
Q

what is the sarcolemma?

A

membrane surrounding the cardiomyocyte

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13
Q

what structures does the sarcolemma also dip into?

A

T-tubules

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14
Q

what provides a ready supply of ATP to sustain contraction?

A

mitochondria

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15
Q

name 2 contractile proteins

A
  • actin

- myosin

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16
Q

what is the name of the essential contractile unit of a cardiomyocyte?

A

sarcomere

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17
Q

what are sarcomeres made up of?

A

actin and myosin

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18
Q

how many sarcomeres roughly are there end-to-end in a cardiomyocyte?

A

around 50

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19
Q

what are Z lines attached to?

A

the thin filaments = actin

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20
Q

what do the thin filaments form a sandwich with?

A

myosin thick filaments

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21
Q

label this sarcomere

A
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22
Q

what is the A band generated by?

A

myosin thick filaments

23
Q

what is the I band mainly composed of?

A

actin thin filaments

24
Q

what are T-tubules?

A

= transverse tubules

- invaginations of the cell membrane which run into the interior of the cell

25
Q

what do t-tubules do and promote?

A
  • transmit the electrical stimulus rapidly into the interior of the cell
  • promote the synchronous activation of the whole depth of the cell, despite the fact the signal to contract is relayed across the external membrane
26
Q

in what stage of a contraction do calcium levels peak?

A

peak in systole, then come back down to baseline in diastole

27
Q

what is the trigger for contraction?

A

a rise in intracellular (cytosolic) Ca++ in the cardiomyocyte

28
Q

what is meant by the term excitation-contraction coupling?

A

the Ca++ dependent pathway via which electrical activation of the myocyte induces contraction

29
Q

Ca++ intracellular levels at rest (diastole) vs in contraction (systole)

A

at rest: 100nM

in contraction: 1uM = MUCH HIGHER

30
Q

what is an action potential (AP)?

A

the transient depolarisation of a cell as a result of ion channel activity

31
Q

the relationship between AP and contraction — explain this diagram (1-5)

A
  1. voltage-gated Na+ channels open
  2. Na+ inflow depolarises the membrane and triggers the opening of more Na+ channels — creates a +ve feedback cycle and a rapidly rising membrane voltage
  3. Na+ channels close when the cell depolarises, and the voltage peaks at nearly +30mV
  4. Ca++ entering through slow calcium channels (L-type) prolongs depolarisation of membrane, creating a plateau — plateau falls slightly because of some K+ leakage, but most K+ channels remain closed until end of plateau
  5. Ca++ channels close and Ca++ is transported out of cell. K+ channels open and rapid K+ outflow returns membrane to its resting potential
32
Q

when the AP is triggered and Ca++ enters the cell, what then happens to induce a contraction?

A
  • Ryanodine receptors open = calcium induced calcium release — calcium can flood out of the sarcoplasmic reticulum, causing this rise in intracellular calcium levels (that we can measure with the calcium transient)
  • calcium then binds to the contractile machinery and we get contraction of the heart
33
Q

where are RyRs located?

A

on the sarcoplasmic reticulum membrane

34
Q

what needs to occur between filaments in order for a contraction to happen?

A

cross bridges need to form between filaments

35
Q

what 3 things is the thin filament composed of?

A
  • actin
  • tropomyosin
  • troponin complex — made up of 3 cardiac specific proteins = cTnT, cTnC, cTnI (cardiac troponin)
36
Q

what is the thick filament composed of?

A
  • myosin
  • hinged stalk
  • globular head
37
Q

what happens when calcium binds to cTnC?

A

it induces a rearrangement in the troponin-tropomyosin complex

38
Q

what is the effect of the rearranged of the troponin-tropomysoin complex, leading to contraction?

A

movement of tropomysoin exposes a myosin binding site on actin, allowing the globular head of the myosin to bind to it, resulting in cross-bridge formation and shortening of the sarcomere —> CONTRACTION

39
Q

what does the binding of calcium to cardiac troponin c regulate?

A

the contractile state of the cardiomyocyte

40
Q

for relaxation to occur what do we need to happen?

A

calcium levels to come back down to baseline

41
Q

where does the majority if the Ca++ need to re-enter?

A

the sarcoplasmic reticulum

42
Q

what does Ca++ enter the SR through?

A

a protein called the sarcoplasmic ATPase (SERCA)

43
Q

what regulates the action of sarcoplasmic ATPase (SERCA)?

A

an additional protein called phospholamban

44
Q

where else does Ca++ get transported into and why?

A

into mitochondria as Ca++ is very important for mitochondrial function

45
Q

what 2 ways is the equivalent of the Ca++ that entered the cell through the LTCC removed?

A
  • either via the sodium calcium exchange (swaps calcium for sodium)
  • or it goes out throguh the plasma membrane calcium ATPase (PMCA)
46
Q

what would the relationship between Ca++, contraction and AP look like on a graph?

A
47
Q

DIASTOLE: explain phase 1 and phases 5-7

A

phase 1:

  • atrial depolarisation — P wave
  • both atria contract — ventricles full

phases 5-7:

  • ventricles are relaxed
  • mitral and tricuspid valves open
  • blood flows passively from atria into ventricles
48
Q

what is LVEDV roughly in an adult heart?

A

120ml

49
Q

in what stage of the cardiac cycle do the ventricles contain the full amount of blood?

A

end of diastole

50
Q

SYSTOLE: explain phase 2 and phases 3-4

A

phase 2:

  • AV valves close
  • ventricles contract, pressure increases, volume unchanged = isovolumetric contraction
  • ventricular depolarisation = QRS complex

phases 3-4:

  • outflow valves open
  • blood ejected into aorta and pulmonary artery
  • volume decreases = LVESV
51
Q

what is LVESV in an adult heart?

A

50ml

52
Q

what is it called when there is no change in volume of blood as all of the valves are shut?

A

isovolumetric contraction

53
Q

what ion channel is responsible for the plateau phase of the ventricular AP? why is the plateau relatively stable?

A

= L-type Ca++ channel
- the LTCC is an inward current, so depolarises the membrane in competition with the repolarising K+ channels (outward currents), therefore creating a plateau where the MP is relatively stable

54
Q

describe what is happening with the cardiac valves at points A, B, C, D

A 
A = mitral valve closes — LVEDV
B = aortic valve opens 
C = aortic valve closes — LVESV
D = mitral valve opens

PBL SEM 2 (44 decks)

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