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CV System - Alex's Cards (ESA2) > Session 4 Lectures > Flashcards

Session 4 Lectures Flashcards

1
Q

What sets the resting membrane potential in cardiac myocytes?

A

Potassium permeability

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2
Q

What is the intra and extracellular concentration of potassium in a cardiac myocyte?

A

4mmol extracellular

140mmol intracellular

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3
Q

Does resting membrane potential reach potassium equilibrium in a cardiac myocyte? (Ek)

A

No not quite
Ek = around -95mv and RMP = -85mv
This is because there is small permeability to other ions at rest

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4
Q

What ion generates contraction?

A

Calcium ions

Need for actin and myosin interaction

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5
Q

What is another term for the cardiac action potential?

A

The ventricular action potential

These are action potentials generated in non-nodal cells eg purkinje fibres

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6
Q

In ventricular action potentials - what stage number is rest and which is the plateau phase?

A

Rest = stage 4
Plateau phase = stage 2

Upstroke (depolarisation) = stage 0
Start of repolarisation = stage 1
Plateau phase = stage 2
Repolarisation = stage 3

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7
Q

What happens to VG sodium channels after opening?

When can they re-open?

A

They inactivate

When at negative membrane potential they close again and can be reopened

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8
Q

How long does diastole last compared to systole?

A

Diastole is 2/3 of time

Systole is 1/3 of time

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9
Q

What are the x and y axis when labelling the ventricular action potential?

A

x axis = Time (ms)

y axis = Membrane potential (Mv)

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10
Q

In cardiac action potential what causes upstroke?

A

Opening of VG Na+ channels (fast acting) and influx of Na+

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11
Q

What causes the plateau phase?

A

Opening of VG Ca2+ channels (Ca2+ influx) and K+ channels also being open (K+ efflux)
They are balanced so plateau

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12
Q

Do cardiac myocytes have more than one type of K+ channel?

A

Yes

Don’t need to know them all yet

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13
Q

What is another term for the pacemaker action potential?

A

The SA node action potential

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14
Q

What is unusual about the pacemaker cells?

A

They never sit at rest and spontaneously depolarise

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15
Q

What is the difference between HCN channels and VG Na+ channels?

A

HCN channels = cause gradual depolarisation of pacemaker cells (in SA node)
They are slow opening Na+ channels

VG Na+ channels = generate action potential in cardiac cells (ventricular action potential)
They are fast opening Na+ channels

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16
Q

What is the pacemaker potential?

A

Gradual opening of HCN channels (funny current) and gradual influx of Na+

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17
Q

What is the membrane potential in the SA node?

What is the resting membrane potential?

A

Membrane potential around -60mV

There is no resting membrane potential - the cells are never at rest

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18
Q

What drives the action potential in the SA node?

A

Opening of L type VG calcium channels

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19
Q

What membrane potential do VG Na+ channels need to reach before opening/activated?

A

Membrane potentials that are more negative than -50m/v

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20
Q

What does HCN channels stand for?

A

Hyperpolarisation-activated, Cyclic Nucleotide-Gated channels

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21
Q

Are the cells in the AV node the name as the SA node?

A

Yes they also spontaneously depolarise and have no resting membrane potential
However the SA node depolarises quicker - this is why it sets the rhythm

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22
Q

What is bradycardia?

A

When action potentials fire too slowly (decreased heart rate)

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23
Q

What is asystole?

A

When action potentials fail to fire - no heart beat

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24
Q

What is tachycardia?

A

When action potentials fire too quickly (increased heart rate)

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25
Q

What happens if electrical activity becomes random?

A

You get fibrillation

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26
Q

What is the normal range for K+ plasma concentration?

A

3.5-5.5 mmol

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27
Q

What is hypokalaemia?

A

Low potassium plasma concentration (less than 3.5 mmol)

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28
Q

What is hyperkalaemia?

A

A high K+ plasma concentration

Over 5.5 mmol

29
Q

What is the effect on membrane potential in hyperkalaemia?

A

The membrane potential becomes less negative - depolarises slightly

30
Q

Why does hyperkalaemia slow the upstroke of the action potential?
(2 reasons)

A
  1. Increased extracellular K+ = membrane potential slightly depolarised (less negative)
    You reduce the driving force for K+ efflux
  2. Some of the VG Na+ channels are inactivated which also slows upstroke
31
Q

What K+ plasma concentration is severe hyperkalaemia?

A

Over 6.5 mmol

Normal = 3.5-5.5mmol

32
Q

What are two possible treatments for hyperkalaemia?

A

Calcium gluconate - this makes the heart less excitable

Give insulin and glucose - promotes K+ moving into cells

33
Q

Explain why hypokalaemia leads to a lengthened action potential and delays in depolarisation

A

Hypokalaemia = decreased extracellular K+ levels
Means there is an increased concentration gradient
K+ slower to move back into the cell and repolarise
L-type Ca+ channels also work best at negative membrane potential so remain open for longer

34
Q

What can a longer action potential lead to?

A

Early after depolarisations

This can lead to oscillations in membrane potential and ventricular fibrillation

35
Q

In a cardiac myocyte, what % of calcium for contraction is received extracellularly?

A

25% across the plasma membrane

75% of the calcium comes from the sarcoplasmic reticulum (via CICR - ryanodine receptors)

36
Q

What does Ca2+ bind to in order for contraction to occur?

A

It binds to troponin C
-Troponin complex sits on top of tropomyosin and winds around the actin filament
When calcium binds it causes a conformational change - tropomyosin is moved out the way to allow myosin to bind at the binding site on the actin filament

37
Q

What does most the Ca2+ go during relaxation of cardiac myocytes?

A

Into the sacroplasmic reticulum via SERCA

38
Q

In the vascular system where is the smooth muscle and which vessel has the most?

A

In the tunica media layer of blood vessels

Arterioles have the most

39
Q

In vascular smooth muscular cells - what 2 ways can Ca2+ levels be increased?

A
  1. Depolarisation of VG Ca2+ channels

2. Noradrenaline or adrenaline activating alpha 1 q (GPCR) resulting in IP3 acting on IP3R and SR Ca2+ release

40
Q

In vascular smooth muscle cells - what does Ca2+ bind to and what does this do?

A

It binds to calmodulin
Calmodulin activates MLCK (myosin light chain kinase) which phosphorylates the light chain on the myosin head - allowing myosin to bind with actin

41
Q

What enzyme in smooth muscle cells inactivates the acting of myosin on actin (contraction)?

A

Myosin light chain phosphatase

42
Q

Can myosin light chain kinase be phosphorylated itself? What happens when it is?

A

Yes it can

When this happens it inhibits its ability to phosphorylate the myosin light chain and inhibits contraction

43
Q

What can phosphorylate myosin light chain kinase to inhibit contraction?

A

Protein kinase C

44
Q

What is a nicotinic receptor?

A

A ligand gated ion channels
All pre-ganglionic receptors are nicotinic
Most post-ganglionic receptors of sympathetic nervous system are nicotinic

45
Q

Give a location where Ach is used as a post-ganglionic neurotransmitter rather than NA (in sympathetic nervous system)

A

Sweat glands

46
Q

What are the 2 divisions of the autonomic nervous system &a where do their pre-ganglionic roots emerge from?

A
  1. Sympathetic (sacral and cranial)

2. Parasympathetic (lumbar and thoracic)

47
Q

For sympathetic and parasympathetic nervous system - which receptors affect pupil of eye and what do they do?

A

Sympathetic = a1 receptor
Dilates the pupil
Parasympathetic = m3 receptor
Constricts the pupil

48
Q

For sympathetic and parasympathetic nervous system - which receptors affect lungs and what do they do?

A

Sympathetic = b2 receptor
Relaxes lungs
Parasympathetic = m3 receptor
Constracts lungs

49
Q

For sympathetic and parasympathetic nervous system - which receptors affect heart and what do they do?

A

Sympathetic = b1
Increased rate and force of contraction
Parasympathetic = m2
Decreased rate and force of contraction

50
Q

For sympathetic and parasympathetic nervous system - which receptors affect sweat glands and what do they do?

A

Sympathetic = a1
Localised secretion
Parasympathetic = m3
Generalised secretion

51
Q

What happens if you denervate the heart?

A

It will continue beating - as the pacemaker cells spontaneously depolarise
The heart will beat more quickly as it is usually under vagal control (of parasympathetic nervous system)

52
Q

What are the postganglionic receptors of parasympathetic nervous system and what do they do?

A

M2 receptors

Decreases heart rate and decreases speed of AV node conduction

53
Q

Where are the main sites of parasympathetic innervation in the heart? (postganglionic cells?)

A

The SA and AV node

54
Q

Where do the preganglionic fibres of parasympathetic nervous system in heart come from?

A

The 10th cranial nerve - the vagus nerve

55
Q

Where are the majority of sympathetic postganglionic cells in the heart?

A

In the SA node, AV node or myocardium (muscular tissue of heart)

56
Q

Where the CV control centre located?

A

Within the medulla oblongata of the brain stem

57
Q

What are baroreceptors? Where are they located?

A

They measure the arterial blood pressure

In carotid sinus and arch of aorta

58
Q

How does NA increase force of contraction?

A

NA acts on B1 receptors which cause an increase in cyclic AMP - activating PKA
This leads to phosphorylation of Ca2+ channels and increased entry of Ca2+ during plateau phase
There is an increased uptake of Ca2+ in SR and increased sensitivity of contractile machinery to Ca2+

59
Q

What receptors do most arteries and veins have - are they innervated by sympathetic or parasympathetic nervous system?

A

Most have a1 receptors (some also have b2)

Most vessels therefore receive sympathetic innervation

60
Q

What does the vasomotor tone allow?

A

Vasodilation of vasoconstriction depending on level of sympathetic output

61
Q

Where might you find blood vessels with a1 and b1 receptors?

A

Liver
Skeletal muscle
Myocardium

62
Q

At physiological concentration which receptor in vasculature will adrenaline prefer to bind to?

A

b2 - they are more sensitive to adrenaline than a1 which is in all vessels

63
Q

What neurotransmitter binds to a1 receptors in vasculature?

A

Noradrenaline
At very high concentrations adrenaline will also bind here (but it prefers to bind to b1 receptors at physiological concentration)

64
Q

Activating b1 receptors on smooth muscle vasculature causes what?

A

Vasodilation
B2 = Ga (s) GPCR
Causes increases in cAMP - activates PKA which opens potassium channels and inhibits MLCK needed for contraction (so relaxation occurs)

65
Q

Activating a1 receptors on smooth muscle vasculature causes what?

A 
Vasodilation 
A1 = Ga(q) GPCR
Stimulates IP3 production 
Acts on IP3R on SR
increase in Ca2+ release from stores = contraction of muscle
66
Q

What causes the largest vasoconstriction effect of smooth muscle vasculature?

A

Increase in local metabolites eg K+, H+ and CO2

67
Q

What type of nerves control input to medulla oblongata?

A

Afferent nerves

68
Q

What do sympathimimetic drugs do?

A

Mimic the sympathetic nervous system e.g. alpha or beta adrenoreceptor agonist

69
Q

Give a few examples of alpha and beta adrenoreceptor antagonist drugs

A
  1. Prazosin (for hypertension) - A1
  2. Propanolol (slows HR and force of contraction but also acts on bronchial smooth muscle to cause vasoconstriction) - non selective B1/2
  3. Atenolol (slows HR and force of contraction) - B1

CV System - Alex's Cards (ESA2) (9 decks)

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