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CVS 2023 > Cellular and molecular events > Flashcards

Cellular and molecular events Flashcards

1
Q

Describe how the resting membrane potential is set up

A

At rest, the membrane of cardiac myocytes are selectively permeable to K+ (open K+ channels)
K+ ions will diffuse down their chemical diffusion gradient (leak) , out of the cell until the chemical gradient is at equilibrium with the electrical gradient.
At this membrane potential, there is no net movement of ions (electrochemical gradient is zero), but there will be a negative membrane potential left inside the cell
The negative membrane potential begins to oppose the further movement of K+ ions outward
This negative membrane potential arises because:

Anions cannot follow, so are left inside the cell
Cell interior becomes negatively charged

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2
Q

What ultimately sets up resting membrane potential?

A

The permeability of cardiac myocytes to K+ ions at rest

Cardiac myocytes permeable at rest

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3
Q

What role does the sodium potassium ATPase have in cardiac RMP?

A
  • Sets up a gradient of ions across the membrane so the concentration of Na+ is lower inside the c ell compared to out side
  • And the concentration of K+ is higher inside the cell, compared to outside.
  • You have a concentration gradient for potassium ions
  • Because at rest, the membrane of. cardiac myocytes is permeable to potassium ions…
  • K+ is high in cell so moves out of cell
  • Makes inside negative relative to outside… (insert RMP membrane generation explain action here)
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4
Q

Equilibrium potential for K+

A

The membrane potential at which electrical and chemical gradients balance (so the electrochemical gradient is zero) and there is no net movement of ions across the membrane.

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5
Q

Why is resting membrane potential not Ek?

A

Because at rest, there is a very small permeability to other ions, not just potassium ions

BUT K+ is main determinant of RMP

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6
Q

Ek vs RMP of ventricular cardiac myocytes

A 
Ek = -95mV
RMP = -80 to -90mV
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7
Q

Special features cardiac myocytes

A
  • They are electrically active, meaning they fire action potentials
  • They are electrically coupled to each other (due to gap-junctions, electrical activity (or depolarisation) is able to spread from one cardiac myocyte to a neighbouring cardiac myocyte and they spread throughout the heart as a whole)

(so if you get depolarisation in one part of the heart, it will spread throughout the heart because all the myocytes are electrically coupled to each other)

Electrically coupled to allow syncronized contraction

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8
Q

What triggers action potential?

A

Depolarisation

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9
Q

What do action potentials trigger? Why is this needed?

A
  • Increase in concentration of Ca2+ in cytoplasm of the cell
  • An increase in this calcium is needed to allow actin and myosin interaction
  • That interaction/sliding of actin and myosin filaments generates the tension/contraction, that allows the heart to pump blood
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10
Q

Whys is Ca2+ required?
What does it bind to?

A

Allows actin and myosin interaction (binds to Troponin C)

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11
Q

How long are action potentials in the axons, skeletal muscles, Sino-atrial node and cardiac ventricle? Draw the intracellular recording of action potentials for each one

A

SA node and Cardiac ventricle have much longer durations of action potentials than axons/skeletal muscle

(the heart has longer durations of action potentials)

100ms vs 0.5ms

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12
Q

Describe the Ventricular cardiac action potential (for my understanding in detail)

A

Background: Ek is quite negative (around -95mV) and so is the RMP (around -80 to -90mv)

The RMP is due to background K+ channels open at rest

Cardiac myocytes are electrically coupled, so if you get depolarisation spreading from neighbouring myocyte to ventricular myocyte, you get a very rapid depolarisation and then opening of Voltage gated sodium channels

Voltage gated sodium channels open with depolarisation, causing upstroke

The sodium equilibrium potential is very positive

So when the Voltage gated sodium channels open, it drives the membrane potential towards the sodium equilibrium potential

it doesn’t get to Ena because you get an inactivation of sodium channels and an opening of some potassium channels

The potassium ions start to move out of the cell, as the k+ ion channels are open and you get get a slight repolarisation

Then you get a long plateau, due to opening of voltage gated calcium channels and some k+ channels also open (calcium channels open more slowly) .

Due to this opening, you get an influx of calcium into the cells/myocytes and a tiny bit of potassium out. The calcium is not driving the cell that positive because its balanced with the potassium

Calcium channels inactivate and voltage gated potassium channels open

This drives the membrane potential back down towards the potassium equilibrium potential

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13
Q

Draw and describe the changes in membrane potential and ionic currents in the ventricular cardiac action potential

A
  1. Spread of depolarisation from neighbouring cells to cardiac myocytes in ventricle to threshold-led potential
  2. VGSC (voltage-gated Na+ channels) open allowing influx of Na+ causing rapid depolarisation
  3. Transient K+ efflux once AP is generated causing slight repolarisation
  4. VGCC (voltage-gated Ca2+ channels) open causing influx of Ca2+ which slows down repolarisation (as Ca2+ influx negates the K+ efflux)
  5. VGCC inactivate and more voltage-gated K+ channels (VGKCs) open causing rapid repolarisation, returning to the RMP
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14
Q

Draw and describe the PHASES of the ventricular cardiac action potentia

A

ps. phase 1 is the initial transient repolarisation

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15
Q

What causes depolarisation?

A

Opening of V gated Na+ channels

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16
Q

What causes slight dip in membrane potetial? (initla repolarisation)

A

Transient outflow of K+

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17
Q

What sustains plateau phase?

A

Open V gated Ca2+ channels

some K+ channels are open

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18
Q

What causes repolarisation?

A

Ca2+ channels inactivate

V gated K+ channels open - K+ moves out

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19
Q

3 phases of Ventricular action potential

A

0 = Na+ influx
1 = initial transient repolarisation
2 = Ca2+ influx (K+ efflux)
3 = K+ efflux

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20
Q

SA node action potential difference

A

No stable Resting membrane potential
Slow depolarisation after each cycle
Na+ doesn’t cause fast depolarisation - Ca2+ does

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21
Q

3 phases of SA node action potential

A 
Pacemaker potential (If - funny current) from influx of Na+ (slow depolarisation)
Opening of V gated Ca2+ channels (fast depolarisation)
Opening of V gated K+ channels (repolarisation)
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22
Q

Pacemaker potential job

A

Initial slope to threshold - funny current (If)

Activated at negative membrane potentials (lower than -50mV) - more negative more activation

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23
Q

How does SA node achieve transient inflow of Na+?

A

HCN channels
Hyperpolarisation-activated Cyclic Nucleotide-gated channels
allow influx of Na+

24
Q

Types of Ca2+ channels SA node

A

L-type and Transient (T ) type

25
Q

How is upstroke achieved SA node?

A

Opening of V gated Ca2+ channels

26
Q

How is down stroke (repolarisation) achieved in SA node?

A

Opening V gated K+ channels (leaves)

27
Q

Innervation SA node

A

No innervation needed

Natural automaticity

28
Q

Membrane potential SA node

A

UNSTABLE (pacemaker potential, funny current)

29
Q

Action potentials through heart speed

A

SA node = fastest

30
Q

Action potential journey

A 
SA node 
Across atria
AV node
Bundle of His
Purkinje fibres 
Ventricle contraction
31
Q

Pacemaker of heart?

A

SA node

sets rhythm

32
Q

AP’s through heart

A

SA node and AV node - fast

Atrial muscle, ventricular muscle and purkinje fibres - slower

33
Q

What is responsible for contraction?

A

Spread of action potential

34
Q

Problems with action potential firing

A

too slow - bradycardia
fail - asystole
too quickly - tachycardia
random - fibrillation

35
Q

Hyperkalaemia

A

High plasma conc (>5.5mmol/L)

36
Q

Hypokalaemia

A

Low plasma conc (<3.5mmol/L)

37
Q

why are cardiac myocytes sensitive to change in K+?

A

k+ permeability dominates membrane potential

38
Q

Hyperkalaemia effects

A

Ek = less negative
Membrane potential depolarises
Inactivates some of Na+ channels
Slows upstroke

39
Q

Risks hyperkalaemia

A

Heart stops - asystole

Initial increase in excitability (depolarised)

40
Q

Extent hyperkalaemia

A

Mild: 5.5 - 5.9 mmol/L
Moderate: 6.0 - 6.4 mmol/L
Severe: > 6.5mmol/L

41
Q

Treatment hyperkalaemia

A

Calcium gluconate
Insulin and glucose

(causes cells to uptake K+)
**Heart needs to be pumping

42
Q

Effects of hypokalaemia

A

Lengthens action potential

Delays repolarisation

43
Q

Problems hypokalaemia

A

Longer action potentials can cause Early After Depolarisation (EAD’s)
Oscillations in membrane potential
Ventricular fibrillation

(remember shaking in hypothermia like osscilations)

44
Q

Excitation contraction coupling initial step

A

Depolarisation opens L type Ca2+ channels in T tubules

45
Q

What does Ca2+ entering cytosol cause in cardiac cells?

A

Opens Calcium induced calcium release (CICR) channels in SR

46
Q

What happens after CICR channels open?

A

Ca2+ binds to troponin C
Conformational change shifts tropomyosin
Binding site revealed on actin = myosin can bind

47
Q

How do cardiac myocytes relax?

A

Ca2+ pumped into SR (via SERCA)

Some exits via membrane (Ca2+ATPase, Na+Ca2+ exchanger)

48
Q

How is tone of blood vessels controlled?

A

Contraction and relaxation of vascular smooth muscle cells

tunica media, arteries arterioles and veins

49
Q

Excitation contraction coupling smooth muscle cells initial stimulation

A

Noradrenaline activates a1 receptors

or depolarisation opening V gated Ca2+ channels

50
Q

What does a1 receptor do?

A

Activates Gaq to produce second messanger IP3

51
Q

What does IP3 do?

A

Binds to receptors on sarcoplasmic reticulum

Initiates release of Ca2+

52
Q

What does Ca2+ once released from cell? (smooth muscle)

A

Binds to calmodulin

53
Q

what does calmodulin do?

A

Activates Myosin light chain kinase (MLCK)

54
Q

What does MLCK do?

A

Phosphorylates myosin light chain = allows interaction with actin

55
Q

How does contraction stop in smooth muscle?

A

Myosin light chain phosphatase dephosphorylates the myosin light chain

PKA phosphorylates myosin light chain kinase = inactive

56
Q

How is contraction inhibited? (smooth muscle cell)

A

PKA (protein kinase A) phosphorylates MLCK and inhibits it

57
Q

Cardiac muscle vs smooth muscle excitation and contraction

A

Cardiac:
Action potential allow Ca2+ entry
More Ca2+ then comes from SR
Ca2+ binds to TROPONIN C

Smooth muslce:
Depolarisation/activation of a-adrenoreceptors
Increased intracellular Ca2+
Ca2+ binds to Calmodulin
Activates MLCK - phosphorylates myosin light chain

CVS 2023 (26 decks)

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