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ESA 2 > CVS 4.1 - Cellular and Molecular Events of the Cardiovascular System > Flashcards

CVS 4.1 - Cellular and Molecular Events of the Cardiovascular System Flashcards

1
Q

What is the resting membrane potential of cardiac myocytes?

A

-90mv

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2
Q

What sets the resting membrane potential of cardiac myoctyes?

A
  • Na+K+ATPase (establishes the gradient)

- Permeability of the membrane to K+ ions

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3
Q

How does Na+K+ATPase establish the gradient?

A
  • Pumps out 3Na+ for every 2K+ pumped in (against gradients)

- Ensures there is always a +1 charge moving out so less ATP than expected is required

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4
Q

What would happen if Na+K+ATPase became blocked?

A
  • Cell would become hyperpolarised due to the leakage of K+
  • Increased number of closed Na+ channels causes a build up inside the cell
  • NCX would become less effective which would increase cytosolic Ca2+
  • Longer action potential as depolarisation would be sustained
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5
Q

How does the membrane’s permeability to K+ ions contribute to the resting membrane potential of cardiac myocytes?

A
  • K+ channels are open at rest so ions flow out down their gradient
  • Intracellular charge is negative relative to the outside due to the positivity of K+
  • K+ is the attracted to the -ve inside of the cell so flows in down its electrical gradient
  • Gradients become balanced so there is no net movement of ions (Ek)
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6
Q

What causes the difference between RMP and Ek?

A

Permeability of the membrane to other ions

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7
Q

What happens to cause depolarisation of the ventricles?

A

Voltage gated Na+ channels open causing the membrane potential to move closer to Ena and therefore to threshold

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8
Q

What happens after the ventricles have depolarised?

A
  • K+ voltage gated channels open

- Initial repolarisation due to the outward flow of K+

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9
Q

What happens after the initial repolarisation of the ventricles?

A
  • Na+ channels deactivate
  • Voltage gated Ca2+ channels (L-type) open causing a Ca2+ influx
  • There is some K+ efflux
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10
Q

What causes the long plateau of the cardiac action potential?

A
  • Ca2+ channels take longer to activate

- Causes long plateau due to prolonged depolarisation

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11
Q

What happens after the long plateau during the cardiac action potential?

A
  • Increased intracellular Ca2+ caused CICR
  • Cardiac myocytes contract
  • Further efflux of K+ moves membrane potential further towards Ek
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12
Q

What is the funny current?

A

The long, slow depolarisation of the SAN

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13
Q

What causes the funny current?

A
  • HCN channels/ Slow Na+ channels
  • Become activated when the membrane potential becomes more negative than -50mv (hyperpolarisation)
  • More negative = more activated
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14
Q

What happens in the SAN when the threshold is reached by the funny current?

A
  • Voltage gated Ca2+ channels open

- Slow depolarisation due to Na+ being deactivated

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15
Q

How does the SAN repolarise?

A
  • Voltage gated K+ channels open

- Repolarisation is caused due to K+ efflux

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16
Q

How do action potentials differ in the ventricles?

A
  • Slower depolarisation

- Depolarisation is caused by opening of voltage gated Na+ channels

17
Q

How do action potentials differ in the SAN?

A
  • Reaches threshold first = faster depolarisation
  • Sets rhythm
  • Opening of Ca2+ channels causes depolarisation
18
Q

What causes CICR from the sarcoplasmic reticulum during the action potential?

A
  • Depolarisation of cardiac myocytes = L type voltage gated channels open causing a calcium influx
  • T tubules are lined with L type channels
  • Localised calcium entry into the cell causes CICR channels on the SR to open
  • Increased localised calcium entry
19
Q

What is the significance of the calcium influx into the myocyte?

A

Sustains depolarisation = longer action potential

20
Q

How does the Ca2+ influx cause contraction of the cardiac muscle?

A
  • Extracellular Ca2+ and Ca2+ from the SR bind to troponin C in the muscle
  • Causes a conformational change which moves tropomyosin out of the actin binding site
21
Q

What is the sliding filament theory?

A
  • Tropomyosin is moved out of the actin binding site by troponin C
  • Allows a myosin actin cross bridge to form
  • Myosin dissociates from ADP + Pi and flexes
  • Causes a power stroke as the myosin moves to a relaxed state
  • ATP binds to myosin head causing it to dissociate from the actin
22
Q

What are the three subunits of troponin and what are their functions?

A
  • Troponin C - Ca2+-binding subunit
  • Troponin I - inhibits ATP-ase activity of acto-myosin
  • Troponin R - tropomyosin-binding subunit which regulates the interaction of troponin complex with thin filaments
23
Q

What happens if Ca2+ and ATP are still available after the muscle has contracted?

A
  • Process repeats

- Can lead to tetany

24
Q

What is tetany?

A

Muscle spasms that occur at irregular intervals

25
Q

What determines the force generated by the cardiac muscle when contracting?

A
  • Number of cross bridges formed

- Cytosolic Ca2+ concentration

26
Q

What causes diastolic dysfunction?

A
  • Higher than normal Ca2+ levels

- Leads to an increase in force of contraction and plateau time

27
Q

What causes systolic dysfunction?

A
  • Lower than normal Ca2+ levels

- Leads to a decrease in force of contraction

28
Q

What is systolic dysfunction?

A

Decrease in myocardial contractility

29
Q

What is diastolic dysfunction?

A

Increase in myocardial contractility

30
Q

What happens when the cardiac muscle relaxes after contraction?

A
  • Ca2+ levels are returned to resting levels
  • 75% is pumped back into the SR by SERCA
  • 25% is pumped out into the extracellular space by NCX/Ca2+ATPase
31
Q

What is tetanus? Does it affect cardiac muscle?

A

An infection that causes muscle spasms. It does not affect cardiac muscle

32
Q

Why doesn’t tetanus affect cardiac muscle?

A
  • Cardiac muscle has a long absolute refractory period due to inactivation of Na+ channels during the plateau
  • Can’t depolarise again so can’t transmit an action potential
  • Less CICR = fewer contractions
33
Q

How is tetany caused?

A
  • Stimulus acts before the previous contraction finishes

- Get multiple action potentials without a refractory period

34
Q

How is contraction of vascular smooth muscle caused?

A
  • Noradrenaline binds to alpha-1 adrenoceptors coupled to Gq proteins
  • Gq breaks down PIP2 into IP3 and DAG in the membrane
  • IP3 causes increased calcium release from the SR
  • 4Ca2+ binds to calmodulin which activates MLCK
  • MLCK phosphorylates myosin light chain = enables myosin-actin cross bridges to form
35
Q

How is contraction of the vascular smooth muscle stopped?

A
  • DAG that is produced from PIP2 along with IP3
  • DAG activates protein kinase C
  • PKC phosphorylates myosin light chain phosphatase = inhibited
36
Q

What is the function of myosin light chain phosphatase?

A
  • Dephosphorylates the myosin light chain

- No longer activated

ESA 2 (63 decks)

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