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CVS * > S4 Electrical and Molecular Events > Flashcards

S4 Electrical and Molecular Events Flashcards

1
Q

What sets up the resting membrane potential in cardiac myocytes?

A
  1. The cells are permeable to K+ at rest
  2. K+ moves out of cell down concentration gradient
  3. This small movement in ions makes the inside negative to the outside
  4. As charge builds up, an electrical gradient is established
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2
Q

How does excitation cause contraction in cardiac myocytes?

A

Cardiac myocytes are electrically active (fire action potentials)

An action potential triggers an increase in cytosolic Ca2+

A rise in calcium is required to allow actin and myosin interactions (generates a contraction (tension))

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3
Q

What are the RMP in an axon, skeletal muscle, SAN and cardiac ventricle?

A

Axon - -70mV
Skeletal muscle - -90mV
SAN - -60mV
Cardiac ventricle - -90mV

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4
Q

What are the stages in a ventricular (cardiac) action potential?

A
  1. Opening of voltage-gated Na+ channels (Na+ influx)
  2. Transient outward K+ current
  3. Opening of voltage gated Ca2+ channels (some K+ channels also open) - plateau (Ca2+ influx and K+ efflux)
  4. Ca2+ channels inactivate, K+ voltage gated channels open (K+ efflux)
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5
Q

What are the stages in a SA node action potential?

A
  1. Pacemaker potential (funny current) - influx of Na+
  2. Opening of voltage-gated Ca2+ channels (upstroke)
  3. Opening to voltage-gated K+ channels - K+ efflux (down stroke)
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6
Q

When is the pacemaker potential activated?

A

When the membrane potentials are more negative than -50mV

The more negative, the more it activates

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7
Q

What are the HCN channels?

A

Hyperpolarisation-activated, Cyclic Nucleotide-gated channels e.g. cAMP

Present in pacemaker potential stage

Allow influx of Na+ which depolarises the cells

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8
Q

What are the channel types involved in the pacemaker potential?

A
  • HCN channels

* Transient (T-type) and L-type Ca2+ channels

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9
Q

What does the natural automaticity mean about the SA node action potential?

A

You don’t need any nervous input to get the action potential started, it is just due to depolarisation of itself

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10
Q

Does the SA node have an unstable or stable membrane potential?

A

Unstable

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11
Q

What does nervous input into the SA node do?

A

Modulates the rate of heart contraction

But the SA node produces an action potential without the nervous input

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12
Q

What is the clinical condition if action potential fire too slowly?

A

Bradycardia (if heart rate is below 60bpm)

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13
Q

What is the clinical condition if action potential fire too quickly?

A

Tachycardia (if heart rate is above 100bpm)

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14
Q

What is the clinical condition if action potentials fail?

A

Asystole

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15
Q

What is the clinical condition if electrical activity becomes random?

A

Fibrillation

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16
Q

When is a plasma K+ concentration considered too high (hyperkalaemia)?

A

If the concentration is above 5.5mmol/L-1

17
Q

When is a plasma K+ concentration considered too low (hypokalaemia)?

A

If the concentration is below 3.5mmol/L-1

18
Q

What are cardiac myocytes so sensitive to changes in the K+ concentration?

A

Because the K+ permeability dominates the resting membrane potential

19
Q

What is the ideal plasma K+ concentration range?

A

3.5 - 5.5mmol/L-1

20
Q

What is the effect of hyperkalaemia on cardiac myocytes?

A

The K+ equilibrium potential gets less negative so the membrane potential DEPOLARISES a bit leading to inactivation of some of the voltage-gates Na+ channels which SLOWS THE UPSTROKE

Ek = 61.5mV (rather than -90mV)

21
Q

What are the risks of hyperkalaemia in terms of cardiac myocytes?

A
  • the heart can stop - asystole
  • may initially increase excitability

Can be mild, moderate or severe (dependent on the concentration)

22
Q

How do you treat hyperkalaemia in terms of cardiac myocytes?

A
  • calcium gluconate (makes the membrane a little less excitable)
  • insulin and glucose - insulin drives K+ into cells and lowers the extracellular K+ level, give with glucose to avoid hypoglycaemia

Treatment only works if the heart hasn’t already stopped

23
Q

What are the effects of hypokalaemia on cardiac myocytes?

A
  • lengthens the action potential

* delays depolarisation

24
Q

What are the problems with hypokalaemia in terms of cardiac myocytes?

A

A longer action potential can lead to early after depolarisations which can lead to oscillations in the membrane potential resulting in ventricular fibrillation

25
Q

Describe how excitation causes contraction in cardiac myocytes.

A
  1. Depolarisation opens L-type Ca2+ channels in the T-tubule system
  2. Localised Ca2+ entry opens CICR channels in the SR (there’s a close link between L-type channels and Ca2+ release channels)
  3. Ca2+ triggers contraction by binding to troponin C
  4. Causing a conformational change which shifts tropomyosin to reveal the myosin binding site on the actin filament
  5. Sliding filament theory
26
Q

How doe cardiac myocytes relax?

A

Ca2+ concentration in the cell must be returned to resting levels - most is pumped back into the SR by SERCA (increased Ca2+ concentration stimulates this pump) and some exits across the cell membrane via sarcolemma Ca2+-ATPase and the NCX

27
Q

What is tone of blood vessels controlled by?

A

By the contraction and relaxation of vascular smooth muscle cells (in the tunica media) - this is present in arteries, arterioles and veins

28
Q

Describe how excitation causes contraction in vascular smooth muscle cells.

A
  1. Depolarisation opens VGCCs
  2. The Gq coupled protein activation releases IP3 and DAG
  3. The IP3 activates release of Ca2+ from the SR
  4. Ca2+ binds to calmodulin (CaM)
  5. CaM + myosin light chain kinase causes phosphorylation of myosin light chain (release ATP)
  6. Phosphorylation of myosin light chain allows binding to actin
  7. Myosin light chain phosphatase (which is constitutively active) then dephosphorylates the chain (using ATP)
  8. However DAG activates PKC which inhibits myosin light chain phosphatase, keeping the myosin light chain in it’s active form for longer
29
Q

How is contraction regulated in vascular smooth muscle cells?

A
  • Ca2+ binding to calmodulin activates myosin light chain kinase
  • relaxation occurs as Ca2+ levels decline as myosin light chain phosphatase dephosphorylates the myosin light chain
  • myosin light chain phosphatase can be phosphorylated by PKA to inhibit the action of myosin light chain kinase - inhibits contraction

CVS * (17 decks)

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