Autonomic Control Of The CVS Flashcards

1
Q

What is the ANS important in regulating?

A

Heart rate
BP
Body temperature
(Homeostasis)

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2
Q

How is the autonomic nervous system divided?

A

Parasympathetic nervous system
Sympathetic nervous system
(Enteric nervous system = sympathetic and parasympathetic fibres)

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3
Q

How long are the pre-ganglionic neurones and post-ganglionic neurones of sympathetic fibres?

A

Pre-ganglionic = Short
Post-ganglionic = Long

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4
Q

How long are the Pre-ganglionic and post-ganglionic neurones of the parasympathetic fibres?

A

Pre-ganglionic = Long
Post-ganglionic = Short

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5
Q

Where do the Preganglionic neurones of the Sympathetic nervous system originate (which part of the spine)?

A

Thoracic lumbar region (Thoracolumbar)

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6
Q

Where do the Preganglionic neurones of the parasympathetic nervous system originate (which part of the spine)?

A

Craniosacral origin

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7
Q

Which post-ganglionic neurone is close to the target tissue, sympathetic or parasympathetic?

A

Parasympathetic post-ganglionic is close to target tissue

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8
Q

What neurotransmitter is released at the end of the pre-ganglionic neurones in both the sympathetic and parasympathetic nervous system?

A

Acetylcholine (ACh)

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9
Q

What receptors are present on the post-ganglionic axon bodies in both the sympathetic and parasympathetic nervous system?

A

Nicotinic ACh receptors
nAChRs

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10
Q

How does binding of ACh to nicotinic acetylcholine receptors affect the receptor?

A

Conformational change opens the ion channel of the receptor
Na+ influx
K+ efflux

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11
Q

What type of receptors are all of the adrenergic (adrenoreceptors)?

A

G protein coupled receptors

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12
Q

What is the neurotransmitter released from the post-ganglionic neurones acting on the effector cells in the Parasympathetic nervous system?

A

Acetylcholine (ACh)

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13
Q

What are the receptors present in the parasympathetic nervous system that are on the effector cells following the post-ganglionic neurones?

A

Muscarinic ACh receptors

NOT NICOTINIC ACh Receptor

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14
Q

How are muscarinic ACh receptors different to Nicotinic ACh receptors?

A

Are G protein coupled receptors

Don’t have ion channels in the receptor like Nicotinic ACh receptors

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15
Q

How many Alpha adrenoreceptors are there?

A

2
Alpha 1 adrenoreceptors
Alpha 2 adrenoreceptors

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16
Q

How many Beta adrenoreceptors are there?

A

3
Beta 1 adrenoreceptors
Beta 2 adrenoreceptors
Beta 3 adrenoreceptors

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17
Q

How many Muscarinic receptors are there?

A

3
M1
M2
M3

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18
Q

How do the sympathetic and parasympathetic nervous system work to maintain a balance together?

A

Sympathetic increases under stress
Parasympathetic increases under basal resting conditions

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19
Q

Where are B1 receptors found?

A

Heart

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20
Q

Where are B2 adrenoreceptors found?

A

Airways of lungs

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21
Q

How does the Autonomic nervous system control the cardiovascular system?

A

Controls:
-Heart rate
-Force of heart contraction
-Peripheral resistance of blood vessels

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22
Q

What is responsible for initiating the electrical activity of the heart?

A

The SAN
NOT the Autonomic Nervous System

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23
Q

What happens to the heart if it is denervated and why?

A

Beats Faster
Not being parasympathetically stimulated by the Vagus nerve which slows the heart (Vagal influence)

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24
Q

What nerve does the parasympathetic input to the heart come from/ where do the pre-ganglionic fibres come from?

A

10th (X) cranial nerve
Also called the Vagus nerve

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25
Q

Where are the post-ganglionic cells located that the vagus nerve (parasympathetic input) interacts with at the heart?

A

SAN
AVN

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26
Q

What receptors does the parasympathetic input to the heart act on and what effects does this have?

A

M2-receptors (muscarinic ACh receptor)

Decreases heart rate = negative chronotropic effect
Decreases AVN conduction velocity/increases time delay initiated

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27
Q

Where are the post-ganglionic fibres of the sympathetic input to the heart innervating?

A

SAN
AVN
Myocardium (This is not innervated by parasympathetic input only sympathetic)

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28
Q

What neurotransmitter is released by the post-ganglionic fibres of the sympathetic input to the heart?

A

Noradrenaline

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29
Q

What receptor does noradrenaline mainly act on in the sympathetic input to the heart?

A

Beta 1 adrenoreceptors

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30
Q

What does activation of the B1 adrenoreceptors in the heart cause?

A

Positive chronotropic effect
Positive Inotropic effect

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31
Q

What is meant by +ve chronotropic effect?

A

Increases heart rate

32
Q

What is meant by +ve inotropic effect?

A

Increased force of contraction

33
Q

So where does the sympathetic input to the heart happen?

What receptors are acted on?

A

SAN
AVN
Myocardium

Beta-1 adrenoreceptors

34
Q

Where does parasympathetic input to the heart happen?

What receptors are acted on?

A

SAN
AVN

Muscarinic-2 receptors

35
Q

What are baroreceptors?

Where are they found?

A

Stretch mediated receptors that detect changes in arterial blood pressure

36
Q

How do action potentials take place in the pacemaker region (SAN) of heart?

A

Slow depolarisation (slow Na+ conductance due to HCN channels causing FUNNY CURRENT)

UPSTROKE = Fast opening of Ca2+ (Calcium INFLUX)

DOWNSTROKE = Opening of K+ channels (K+ EFFLUX) Ca2+ channels close

37
Q

How does the sympathetic nervous system affect pacemaker potentials/heart rate?

A

INCREASES heart rate

It increases the speed threshold for an action potential is reached (faster APs)

38
Q

How does the parasympathetic nervous system affect pacemaker potentials/heart rate?

A

Decreases heart rate

It decreases the speed which threshold for an action potential is reached (slower APs)

39
Q

How does sympathetic activity increase the speed by which threshold for an action potential is reached?

A

Noradrenaline binds to Beta 1 receptors
Activates the G protein (Gs) which stimulates adenylate cyclase (enzyme)
Increases the amount of cAMP
More cAMP can act on HCN channels producing a steeper FUNNY CURRENT
Threshold therefore reached quicker = faster heart rate

40
Q

How does parasympathetic activity decrease the speed by which threshold for action potentials are reached slowing heart rate?

A

ACh binds to M2 receptors
G protein activated (Gi) which inhibits adenylyl cyclase (enzyme)
Less cAMP produced
Less HCN channels stimulated so less Na+ moves in, also increased K+ conductance
Therefore take longer for cell to depolarise to threshold potential since takes longer for Na+ to move in through fewer HCN channels

41
Q

How does noradrenaline have a positive inotropic effect on the heart?

A

Binds to Beta-1 receptor
Increases cAMP
cAMP activates PKA (Protein Kinase A)
PKA Phosphorylates Ca2+ channels allowing Ca2+ influx into cell
Influx of Ca2+ causes more Ca2+ to be released from the Sarcoplasmic reticulum
PKA also inhibits Phospholamban which brings Ca2+ back int SR

More Ca2+ in cytoplasm = stronger contraction

42
Q

Do most vessel only have sympathetic innervation or parasympathetic innervation?

A

Sympathetic innervation

43
Q

What receptors do most arteries and veins have?

A

Alpha 1 adrenoreceptors

44
Q

What receptors do coronary and skeletal muscle vasculature have?

A

Alpha 1 + Beta 2

45
Q

What is Vasomotor tone and why is it important?

A

The normal amount that the smooth muscle of the blood vessel is contracted at rest

Allows for vasodilation if it relaxes more
Allows for vasoconstriction if it constricts more

46
Q

How does activation of the alpha 1 (A1) receptor on blood vessels with both A1 and B2 adrenoreceptors affect the blood vessel?

What neurotransmitter activates A1?

A

Vasoconstriction

Noradrenaline

47
Q

What neurotransmitter will preferentially bind to B2 adrenoreceptors in blood vessels with both A1 and B2 at physiological concentrations?

A

Adrenaline

48
Q

What affect does adrenaline binding to B2 have on a blood vessel?

A

Vasodilation

49
Q

What affect does noradrenaline or adrenaline binding to A1 adrenoreceptors have on a blood vessel?

A

Vasoconstriction

50
Q

In blood vessels that have both A1 and B2 receptors, at HIGH concentrations of adrenaline, which receptor will the adrenaline bind to?

What effect does this have?

A

A1
Vasoconstriction

51
Q

In blood vessels that have both A1 and B2 receptors, which receptor will adrenaline preferentially bind to at normal physiological concentrations and what affect does this have?

A

B2

Vasodilation

52
Q

How does Activating B2 adrenoreceptors cause vasodilation of vascular smooth muscle?

A

G protein stimulates Adenylyl cyclase
More cAMP
PKA activated
PKA Phosphorylates MLCK inhibiting it
So MLC not phosphorylated preventing actin myosin interaction (no contraction)

53
Q

How does activating A1 adrenoreceptors cause vasoconstriction?

A

G protein stimulates IP3 (Inositol triphosphate) production
IP3 stimulates SR to release Ca2+
Ca2+ interacts with Calmodulin
Ca2+ - Calmodulin complex activates MLCK
MLCK Phosphorylates MLC allowing myosin head to interact with actin
CONTRACTION

54
Q

What affect do high amounts of metabolites have on vascular smooth muscle?

A

Vasodilation

55
Q

What receptors in the carotid sinus and aortic arch detect increased arterial blood pressure?

A

Baroreceptors

56
Q

What happens when Baroreceptors are stretched detecting increased blood pressure?

A

Fire AP to medulla
Decreased sympathetic stimulation
Vasodilation
Bradycardia

57
Q

What is the baroreceptor reflex?

A

Maintains blood pressure over short periods

Compensates for moment to moment changes in arterial BP

58
Q

What is the problem with the baroreceptor reflex?

A

With hypertension the baroreceptors re-set to a higher level

59
Q

What are the 3 categories of drugs that act on the ANS

A

Sympathomimetics
Adrenoceptor antagonists
Cholinergics

60
Q

What are sympathomimetic drugs?

A

Drugs that enhance the nerves of the sympathetic nervous system

Alpha adrenoreceptor agonists
Beta adrenoreceptor agonists

61
Q

What drug is administered in cardiac arrest and anaphylactic shock?

A

Adrenaline

62
Q

When adrenaline is administered in anaphylactic shock or cardiac arrest, which adrenoreceptor is being activated?

A

Alpha 1 (A1)
Due to higher concentrations of adrenaline compared to normal physiological concentrations

63
Q

When there is cardiogenic shock/pump failure, DOBUTAMINE is given, what type of drug is this?

A

B1 agonist
Sympathomimetic drug

64
Q

What affect does a B1 agonist (dobutamine) have on the heart?

A

Increased heart rate
Increased strength of contraction

65
Q

When someone has asthma they are often treated with SALBUTAMOL, what type of drug is this?

A

B2 agonist
Sympathomimetic

66
Q

How does the B2 agonist salbutamol help treat asthma?

A

Vasodilation of the smooth muscle
Increased cAMP
Inc PKA
MLCK inhibited (K+ influx no Ca2+)
Muscle relaxes

67
Q

What is an example of an alpha adrenoreceptor antagonist?

A

Prazosin

68
Q

What affect does an alpha 1 (A1) antagonist have on the body?
Meachanism of action of Prazosin

A

Prevents noradrenaline binding to smooth muscle A1 receptors
Prevents constriction so vasodilation happens

69
Q

What is a B-adrenoreceptor antagonist that is specifc to B1 receptor?

A

Atenolol

70
Q

What affect does the B1 selective adrenoreceptor antagonist Atenolol have on the body?

A

Affects the heart
Prevents noradrenaline binding to B1
Slows heart rate
Reduces force of contraction

71
Q

Propranolol is a non selective B1/B2 receptor antagonist, what affect will this have on the body?

A

Slows heart
Reduces force of heart contraction
Bronchial smooth muscle contraction (bronchoconstriction)

Prevents noradrenaline binding to the B receptors

72
Q

What are cholinergics?

A

Muscarinic receptor agonists and antagonists

73
Q

How can I remember where the beta adrenoreceptors are found?

A

B1 in heart (only have 1 heart)
B2 in lungs and (have 2 lungs)

74
Q

Where are alpha adrenoreceptors found?

A

Blood vessels

75
Q

What happens to blood vessels when there is:
Increased noradrenaline?
Decreased noradrenaline?

What receptor is being activated more or less?

A

Increased noradrenaline = Vasoconstriction (increased activation of A1)

Decreased noradrenaline = Vasodilation (Decreased activation of A1)