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SGUL - Physiology 1 > Cardiac Contraction > Flashcards

Cardiac Contraction Flashcards

1
Q

What are the effects of positive inotropic agents?

A

Increase myocardial contractility by increasing intracellular [Ca2+]

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2
Q

What are dopamine and dobutamine usually used for?

A

Acute heart failure

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3
Q

Outline a possible mechanism of action for dopamine

A
  • stimulate β-adrenoreceptors on the heart
  • weak stimulation of other adrenoreceptors found in body - so main target is heart
  • similar action to noradrenaline
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4
Q

When is glucagon used clinically?

A
  • Treat acute heart failure
  • Glucagon is used if patient uses beta blockers
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5
Q

Outline a mechanism of action for glucagon

A
  • acts on the heart
  • stimulates Gαs-linked GPCRs ∴increased conversion of ATP to cAMP ∴ increased activation of PKA
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6
Q

What is the purpose of PDE3?

A

TYPE 3 PHOSPHODIESTERASE
- Converts cAMP to ATP ∴ reduced concentration of cAMP ∴ reduced activation of PKA ∴ reduced contractility

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7
Q

Outline the mechanism of action of Amrinone

A
  • Inhibits PDE3
  • Prevents reduction in cAMP concentration ∴ increased activation of PKA ∴ greater phosphorylation of calcium ion channels ∴ greater contractility
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8
Q

What are cardiac glycosides - give an example.

A
  • Increase output force of contraction of heart whilst decreasing rate of contraction through inhibition of the sodium-potassium ATPase exchanger
  • Example - digoxin
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9
Q

Outline the importance of the sodium-potassium ATPase exchanger.

A
  • Draws on energy from ATP hydrolysis
  • For every ATP molecule consumed, 3 sodium ions are exported and 2 potassium ions are imported (maintains sodium ion gradient)
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10
Q

How does the sodium-calcium ion exchanger use the sodium ion gradient?

A
  • Gradient is used to remove calcium ions from inside the cell
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11
Q

Given that digoxin inhibits the sodium-potassium ATPase exchanger, suggest how the sodium-calcium exchanger is affected by digoxin.

A

Increased intracellular [Na+] ∴ reduced gradient and therefore reduced entry of sodium ions through sodium-calcium ion exchanger

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12
Q

How are the calcium ion concentrations affected by digoxin?

A
  • Reduced influx of sodium ions through sodium-calcium ion exchanger
  • Increased intracellular [Ca2+] ∴ increased cardiac contraction
  • Increased [Ca2+] within SR stores ∴ greater CICR ∴ greater force of contraction
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13
Q

Where are the β-adrenergic receptors found?

A
  • Contractile cells of the heart
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14
Q

Briefly outline the structure of the β-adrenergic receptors.

A
  • Made up of a single protein
  • 7 transmembrane domains
  • Linked to a Gαs subunit
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15
Q

Outline the mechanism of action of a beta adrenergic receptor

A
  • Gαs subunit binds to and stimulates adenylate cyclase
  • Increased conversion of ATP to cAMP
  • Increased activation of PKA ∴ calcium ion channels are phosphorylated
  • Increased intracellular [Ca2+] ∴ greater CICR ∴ greater binding to troponin C
  • Greater actin-myosin interactions ∴ greater pacemaker potentials - increased ionotropy and contractility
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16
Q

How does sympathetic stimulation influence the activity of voltage-gated calcium ion channels?

A
  • Increased activity ∴ increased calcium ion influx ∴ increased intracellular [Ca2+]
  • Greater amplitude in plateau phase
  • Greater depolarisation ∴ greater contraction
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17
Q

How does sympathetic stimulation influence sarcoplasmic reticulum Ca2+-ATPase activity?

A
  • Increased activity
  • Increased uptake of calcium ions into SR stores ∴ faster decrease in calcium ion concentration ∴ faster relaxation
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18
Q

How does sympathetic stimulation influence potassium ion channel activity?

A
  • PKA causes these channels to open
  • Faster repolarisation ∴ shorter but faster action potentials but with greater amplitudes in given time∴ greater heart rate
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19
Q

How does sympathetic stimulation influence diastolic time?

A
  • Time stays constant
  • Still needed for filling of chambers with heart and coronary perfusion
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20
Q

Name two ways in which pharmaceuticals can influence cardiac output

A
  • Increase in activity of voltage-gated calcium ion channels ∴ increase intracellular [Ca2+] e.g noradrenaline
  • Reduced expulsion of calcium from cytoplasm ∴ high intracellular [Ca2+] is maintained for longer e.g cardiac glycosides
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21
Q

What is the typical result of increasing [Ca2+]?

A
  • Harder/faster contraction
  • Greater cardiac output
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22
Q

What are the typical effects of calcium blockers and beta blockers?

A
  • Reduced intracellular [Ca2+]
  • Slower contraction
  • Reduced cardiac output
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23
Q

RELAXATION OF CARDIAC MUSCLE - What occurs to the voltage-gated sodium and potassium ion channels?

A
  • Voltage-gated sodium ion channels close
  • Voltage-gated potassium ion channels open
  • Repolarisation occurs
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24
Q

RELAXATION OF CARDIAC MUSCLE - What occurs after repolarisation of the action potential?

A
  • Repolarisation of the T-tubules
  • Closure of the voltage-gated calcium ion channels ∴ reduced influx of calcium ions
  • No CICR from the SR
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25
Q

RELAXATION OF CARDIAC MUSCLE - How does the muscle cells respond to the high calcium ion concentration in the cell?

A
  • Sodium-calcium exchanger removes calcium ions from the cell in exchange for sodium ions
  • Most calcium ions are taken back up into the SR using the sarcoplasmic Ca2+ ATPase (requiring energy)
  • Some calcium ions are taken up by the mitochondria
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26
Q

Define myocardium

A

The muscles found within the central layer of the walls of the heart

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27
Q

What specialised cells is the myocardium made up of?

A

Cardiomyocytes

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28
Q

Outline the difference between inotropy and Starling’s Law.

A

Starling’s Law is intrinsic - inotropy is extrinsic
- Starling’s Law is linked to an increase in volume due to stretch ∴ not linked to a rise in [Ca2+]

29
Q

What does a typical Starling curve tell about filling pressure.

A

Filling pressure on x-axis
- As pressure increases so does the cardiac output
- Greater initial stretch ∴ greater force of contraction up to a certain point - beyond this point, plateaus

30
Q

How does the use of a positive inotropic agent influence a Starling curve?

A
  • Curve shifted upwards so Starling’s law still applies
  • Force of contraction increases
31
Q

Outline the first step of cardiac contraction.

A
  • Action potential initiated at SAN and passed through adjacent cardiomyocytes through gap junctions
  • Activates VGCCs in the T-tubules causing Ca2+ influx into the cardiomyocyte
  • Calcium ions bind to troponin-C in the sarcomere
  • Binding causes conformation of the tropomyosin complex ∴ actin binding sites are exposed
32
Q

Outline the second and third steps of cardiac contraction

A
  • Myosin in high energy form has ADP+phosphate
  • Binds to exposed actin binding site, causing cross bridge to be formed ∴ phosphate released
  • Myosin changes conformation and releases ADP ∴ actin filaments pulled towards centre of sarcomere (i.e powerstroke) . Myosin left in low energy configuration
33
Q

Outline the fourth and fifth steps of cardiac contraction

A
  • Myosin remains bound to actin until binding of ATP causes release from actin
  • ATP hydrolysed to ADP and inorganic phosphate - myosin brought back to high energy form. Head is ‘cocked’ - prepared for another power stroke
  • Cycle repeats along as calcium ions are present and actin binding sites remain exposed
34
Q

Outline the final step of cardiac contraction

A
  • Intracellular Ca2+ removed from SR actively ∴ decrease in [Ca2+]
  • Troponin complex brought back into inhibiting position ∴ myosin can no longer bind
  • Actin filaments return to original position ∴ muscle relaxes
35
Q

What does troponin regulate?

A

Conformation of tropomyosin

36
Q

What are the three subunits that troponin is made up of?

A

Troponin T
Troponin I
Troponin C

37
Q

What does Troponin T bind to?

A

Tropomyosin

38
Q

What does Troponin I bind to?

A

Actin filaments

39
Q

What does Troponin C bind to?

A

Calcium ions

40
Q

Describe the original conformation of tropomyosin (i.e when no calcium ions bound to troponin C)?

A
  • Troponin I brought to active site and binds to actin filaments
  • Prevents binding of myosin to actin
41
Q

What is the clinical significance of the isoforms of Troponin I and Troponin T?

A
  • Released into blood following damage to myocardium e.g following myocardial infarction
  • Used to diagnose MI/ differentiate it from angina
42
Q

What is cardiac contraction dependent on?

A

Increase in intracellular [Ca2+]

43
Q

What are the striations in cardiac muscle a result of?

A

Z-lines

44
Q

What do Z-lines mark?

A

Junction of actin filaments in adjacent sarcomeres

45
Q

What does the relative movement of actin and myosin filaments cause?

A
  • Z-lines brought closer together
  • Muscle fibres shortened during contraction
46
Q

What does calcium ions activate in smooth muscle?

A

Myosin light chain kinase (NOT TROPONIN)

47
Q

What is the sarcoplasmic reticulum?

A

Membrane bound structure in muscle cells that stores calcium ions

48
Q

What is the T-tubule system?

A

Invaginations in the sarcolemma - pass deep into the cardiac muscle cells

49
Q

How do action potentials cause local rising in intracellular [Ca2+] through VGCCs?

A
  • Wave of depolarisation - during action potentials - depolarises T-tubules ∴ activates VGCCs causing calcium influx
49
Q

How do action potentials cause local rising in intracellular [Ca2+] through ryanodine receptors?

A
  • Some calcium ions activate ryanodine receptors found in close proximity to ion channels
  • Causes intracellular calcium release from SR.
  • Local [Ca2+] rises ∴ CICR occurs
50
Q

Why are the T-tubules and RyRs found near the sarcomeres?

A

Allows coordinated link between electrical activity and contraction

51
Q

Outline how cardiac action potentials spread from cell to cell

A

Passes through gap junction-rich intercalated discs

52
Q

What does the passage through intercalated discs allow the action potential to do?

A

Induce depolarisation in adjacent cells
- Allows spread of wave of depolarisation across the heart

53
Q

What ion type facilitate the spreading of cardiac action potentials?

A

Na+

54
Q

Outline a potential diagram fora cardiac action potential

A

SEE SLIDES

55
Q

Outline what occurs during Phase 0 of the cardiac action potential

A
  • Initial depolarisation triggers opening of sodium ion channels ∴ influx of sodium ions
  • Membrane potential becomes more positive
56
Q

Outline what occurs during Phase 1 of the cardiac action potential

A
  • VGCCs open ∴ influx of calcium ions
  • Initial dépolarisation due to action of sodium-potassium exchanger
57
Q

Outline what occurs during Phase 2 of the cardiac action potential

A
  • Plateau phase - calcium influx and CICR from intracellular stores ∴ increase in intracellular [Ca2+]
  • Force of contraction will be proportional to intracellular [Ca2+]
58
Q

Outline what occurs during Phase 3 of the cardiac action potential

A
  • Repolarisation - voltage gated potassium ion channels open and VGCCs close ∴ muscle relaxation
  • Membrane potential becomes less positive ∴ reaches stable resting potential
59
Q

TRUE or FALSE - Calcium rise is part of an all or nothing response during contraction

A

WRONG
- Contraction is concentration-dependent
- Depending on how high [Ca2+] is, there can be greater forces of contraction

60
Q

What is the normal cytosolic calcium concentration during resting phase?

A

0.1 μM

61
Q

During normal contraction, what is the usual calcium concentration?

A

1 μM

62
Q

During strong exercise/fight or flight responses, what is the usual calcium concentration?

A

10 μM

63
Q

What do the intercalated discs contain?

A

Gap junctions

64
Q

What is the purpose of gap junctions during contraction?

A

Allows wave of depolarisation to spread from one cell to next

65
Q

What are the myofibrils made up of?

A

Sarcomeres

66
Q

How do the myofibrils cause contraction?

A

They shorten

67
Q

How do sarcomeres cause contraction?

A

Relative movement of actin and myosin filaments towards each other

SGUL - Physiology 1 (68 decks)

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