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ESA2 LKM > CVS - autonomic system > Flashcards

CVS - autonomic system Flashcards

1
Q

On what basis is the autonomic system divided into parasympathetic and sympathetic?

A

On anatomical grounds - where the spinal nerves exit.

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2
Q

Some textbooks also divide the autonomic nervous system into a third division: sympathetic, parasympathetic and …

A

Enteric nervous system - a network of neurones surrounding the GIT. It is normally controlled by a mixture of parasympathetic and sympathetic fibres.

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3
Q

Describe the general set up of the neurones in the parasympathetic nervous system e.g. start, middle and finish.

A

Two neurones arranged in parallel.

  1. Pre-ganglionic neurone (cell body is in the CNS)
  2. Post-ganglionic neurone
  3. Target cell
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4
Q

Where do the preganglionic neurones arise from in the sympathetic nervous system?

A

Thoracolumbar origin ( T1 to L2 or L3)

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5
Q

Where do the pre-ganglionic and post-ganglionic neurones synapse in the sympathetic nervous system?

A

Most synapse in the paravertebral chain of ganglia but some synapse in a number of prevertebral ganglia (between paravertebral chain and target organ).

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6
Q

Where do the preganglionic neurones arise from in the parasympathetic nervous system?

A

Craniosacral origin ( cranial nerves 3,7,9 and 10; S2-S4)

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7
Q

Where do the cranial nerves arise from?

A

They are twelve pairs of nerves which arise directly from the brain, not from the spinal cord, and pass through separate apertures in the skull.

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8
Q

Where do the pre-ganglionic and post-ganglionic neurones synapse in the parasympathetic nervous system?

A

They synapse with neurones in ganglia close to the target tissues. Then have short post-ganglionic neurones (these can actually be embedded within the wall of the target organ)/

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9
Q

What neurotransmitters are released by the pre-ganglionic neurones and post-ganglionic neurones of the sympathetic system? What receptors are present for these neurotransmitters?

A

Pre-ganglionic: ACh (bind to nAChR)

Post-ganglionic NA (bind to adrenergic receptors)

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10
Q

The sympathetic input to sweat glands is an exception - what type of neurotransmitter does this use?

A

Cholinergic (though some like hands are triggered by adrenaline too).

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11
Q

Describe the specialisations of chromaffin cells of the adrenal medulla:

A

They are specialised postganglionic sympathetic neurones, with no axons. In response to ACh binding to their nAChRs they release adrenaline which circulates in the blood stream.

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12
Q

What type of receptors does adrenaline and noradrenalin e work upon?

A

Adrenoreceptors = G protein-coupled receptors e.g. alpha1,2; beta1,2 (and others)

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13
Q

Why do different tissues have different sub-types of adrenoreceptors? How is this useful to practitioners?

A

This allows them diversity in their actions/response to the same neurotransmitters. This can be used to selectively target drugs to specific tissues.

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14
Q

What co-transmitters can also be released with NA or adrenaline at the synapse of post-ganglionic neurones with effector cells?

A

Neuropeptide Y (NPY) and ATP

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15
Q

What neurotransmitters are released by the pre-ganglionic neurones and post-ganglionic neurones of the parasympathetic system? What receptors are present for these neurotransmitters?

A

Preganglionic - ACh (nAChR)

Post-ganglionic - ACh (mAChR)

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16
Q

What type of receptors are muscarinic receptors?

A

G-protein coupled receptors - unlike nAChR they do not have an integral ion channel

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17
Q

When is the sympathetic system dominant over the parasympathetic system and vice versa?

A

Sympathetic activity is increased under stress.

Parasympathetic system is more dominant under basal conditions.

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18
Q

What is the sympathetic and parasympathetic actions on the pupil of the eye? Which receptors mediate these actions?

A 
Sympathetic = pupil dilation (radial muscle contraction), mediated by alpha-1 receptors
Parasympathetic = pupil contraction (sphincter muscle contraction), mediated by M3 receptors.
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19
Q

What is the sympathetic and parasympathetic actions on the airways of the lungs? Which receptors mediate these actions?

A 
Sympathetic = relaxation of bronichole smooth muscle -> vasodilation of bronchioles, mediated by Beta-2 receptors
Parasympathetic = vasoconstriction, mediated by M3 receptors.
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20
Q

What is the sympathetic and parasympathetic actions on the heart? Which receptors mediate these actions?

A 
Sympathetic = increased chronotropy and ionotropy, mediated by beta-1 receptors
Parasympathetic = decreased chronotropy, mediated by M2 receptors.
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21
Q

What is the sympathetic and parasympathetic actions on the sweat glands? Which receptors mediate these actions?

A

Sympathetic =
1. localised secretion (e.g. palms), mediated by alpha-1 receptors
2. Generalised secretion -> temperature control, mediated by M3 receptors
Parasympathetic = NO EFFECT!

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22
Q

Sympathetic drive to different tissues is independently regulated. When is this not the case?

A

On some occasion (fight and flight) there can be a more co-ordinated sympathetic response.

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23
Q

What does the ANS control in the cardiovascular system?

A
  1. Heart rate
  2. Force of contraction of heart
  3. Peripheral resistance of blood vessels
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24
Q

What is the affect of the ANS on electrical activity in the heart?

A

It does not initiate electrical activity - the heart has its own automaticity (a denervated heart still beats but at a faster rate (~100bpm)). Therefore the parasympathetic NS dominates (vagal influence) at rest -> a decrease in this natural heart rate set by SA cells.

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25
Q

Describe the pre-ganglionic neurones of the parasympathetic input to the heart and where they synapse. What neurotransmitters and receptors do they use?

A

Preganglionic fibres = 10th cranial nerve (vagus). They synapse with the post-ganglionic cells on the epicardial surface or within the walls of the heart at SA and AV node.
Post-ganglionic cells release ACh which acts on M2 receptors.

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26
Q

What is the effect of parasympathetic input at the SA and AV node?

A 
Decreased chronotropy (heart rate)
Decreased AV node conduction velocity (it enhances the natural slowing down of conduction that occurs anyway at the AV node).
27
Q

Describe the pre-ganglionic neurones of the sympathetic input to the heart and where they synapse. What neurotransmitters and receptors do they use?

A

Pre-ganglionic fibres synapse with post-ganglionic at the sympathetic trunk/chain. The post-ganglionic fibres then innervate the SA node, AV node and myocardium. They release NA and act mainly on B1 receptors (B2 and B3 are also present but the main effect is mediated by B1).

28
Q

What is the effect of parasympathetic input at the SA, AV node and myocardium?

A 
Positive chronotropy
Positive ionotropy (force of contraction).
29
Q

Why does the parasympathetic nervous system not cause a change in ionotropy?

A

The parasympathetic NS, unlike the sympathetic NS, does not innervate much myocardium.

30
Q

Where is the cardiovascular centre, that coordinates autonomic control of the heart, situated?

A

Medulla oblongata - lowest part of the brain stem

31
Q

What are the sensory receptors which input information on blood pressure to the cardiovascular centre?

A

baroreceptors in the carotid sinus and arch of aorta

32
Q

What is the pacemaker potential?

A

The slow depolarisation of SA cells by Na+ conductance through HCN channels, called the funny current (I(f)).

33
Q

What causes the upstroke of the SA node action potential?

A

Opening of fast VOCC

34
Q

What causes the downstroke of the SA node action potential?

A
  1. Closing of VOCC

2. Opening of V-gated K+ channels

35
Q

What effect does sympathetic active have on the pacemaker potential?

A

It increase the slope of the pacemaker potential therefore causing faster depolarisation to threshold. Therefore increased chronotropy.

36
Q

What effect does parasympathetic active have on the pacemaker potential?

A

It decreases the slope of the pacemaker potential therefore causing slower depolarisation to threshold. Therfore decreased chronotropy.

37
Q

How does the sympathetic system cause a faster pacemaker potential and therefore increased heart rate?

A
  1. Release of NA from post-ganglionic fibres at the SA binds to B1 receptors
  2. These GPCRs (Gs) cause an increase in cAMP in the SA node cells which bind to and open HCN channels
  3. Faster influx of Na+ occurs and therefore faster depolarisation to threshold.
38
Q

How does the parasympathetic system cause a slower pacemaker potential and therefore slower heart rate?

A
  1. Release of ACh from post-ganglionic neurones at the SA bind to M2 receptors
  2. The beta-gamma subunit of the Gi- protein of these GPCRs increases K+ conductance
  3. The alpha subunit decrease cAMP levels which deactivates HCN channels
  4. Therefore the fewer open HCN channels and increase in K+ conductance out of SA cell, causing a slower rate of depolarisation and therefore a slower action potential.
39
Q

How does the sympathetic system increase inotropy?

A
  1. NA acting on B1 receptors in myocardium causes an increase in cAMP ->activation of PKA
  2. PKA phosphorylates L-type Ca2+ channels, increasing Ca2+ entry during phase 2 of the AP (plateau-phase) and consequently Ca2+ entry from the SER via Ca2+ activated ryanodine receptors
  3. Over several cycles this builds up the Ca2+ store and means that more Ca2+ can be released (and the higher the [Ca2+]the stronger the contraction)
  4. Phosphorylation of phospholamban by PKA stops its inhibition of SERCA, leading to faster Ca2+ uptake, enhancing the amount of Ca2+ in stores and shortening systole.
  5. It also causes an increase in troponin C sensitivity to Ca2+
40
Q

How are most blood vessels innervated by the autonomic NS?

A

By sympathetic innervation - with the exception of some specialised tissues e.g. erectile tissues which have parasympathetic innervation

41
Q

What type of adrenoreceptors are found in most arteries and veins? What about the arteries and veins in coronary and skeletal muscle?

A

Most - alpha-1 receptors

Coronary and skeletal muscle - ALSO have B2 receptors

42
Q

What is vasomotor tone? What determines the vasomotor tone?

A

Is the amount of tension of smooth muscle cells in the walls of blood vessels, particularly arteries. It is determines by the level of sympathetic input to alpha-1 receptors in the smooth muscle. Increased input .-> vasconstriction (increased vasomotor tone). Decreased input -> vasodilation (decreased vasomotor tone).

43
Q

Skeletal muscle, myocardium and the liver have B2 receptors as well as alpha-1 receptors in smooth muscle cells in blood vessel walls. What are the consequences of this?

A

Physiological concentrations of circulating adrenaline has a higher affinity for beta-2 receptors than alpha-1. Binding of adrenaline to beta-2 receptors causes vasodilation

44
Q

How does activation of B2 receptors cause smooth muscle vasodilation?

A
  1. Gs-type GPCR is activated by circulating adrenaline
  2. alpha-s subunit dissociates and activates adenyl cyclase
  3. Activation of adenyl cyclase increases cAMP levels
  4. cAMP inhibits MLCK
  5. Phosphorylation of myosin light chain is decreased which results in a decrease in smooth muscle contraction = vasodilation
45
Q

At high circulating concentrations what receptor, other than B2, will it now bind to?

A

It will bind to alpha-1 receptors (which normally have a higher affinity for noradrenaline).

46
Q

What is the role of local metabolites on vascular tone?

A

They have a strong vasodilatory effect. This is more important for ensuring adequate perfusion of skeletal and coronary muscle than activation of B2-receptors.

47
Q

Name some metabolites which act as local vasodilators:

A

adenosine, K+, H+, increase pCO2.

48
Q

What is the difference in blood pressure detection of baroreceptors and atrial receptors?

A

Baroreceptors detect the high pressure side of the system whereas atrial receptors detect the low pressure side of the system.

49
Q

Describe how the CVS is controlled overall?

A

Changes in the state of the system (detected by baroreceptors and atrial receptors) are communicated to the medullary centers via afferent nerves. Higher centre of the brain also feed into the medullary centers. It alters activity of efferent nerves (sympathetic to blood vessels and sympathetic and parasympathetic to the heart) to change vascular resistance and cardiac output.

50
Q

How do baroreceptors detect changes in blood pressure?

A

They are nerve endings in the carotid sinus and aortic arch. When arterial pressure is increased it stretches these receptors.

51
Q

What is the baroreceptor reflex to an increase in mean arterial pressure?

A
  1. Stretching of the baroreceptors sends signals down afferent pathways to the medulla.
  2. The medulla decreases its sympathetic ouput to the the heart and blood vessels along its efferent pathway
  3. This results in decreased chronotropy and vasodilation.
52
Q

What are sympathomimetrics?

A

They are drugs which mimic the action of the SNS e.g. alpha-adrenoceptor agonists, beta-adrenoceptor agonist

53
Q

What types of drugs act on the ANS?

A
  1. Sympathomimetrics
  2. Adrenoceptor antagonists
  3. Cholinergics (muscarinic agonists and antagonists)
54
Q

Why is adrenaline administrated in a cardiac arrest?

A
  1. Peripheral vasoconstriction ensures that blood is concentrated to the vital organs - brain and heart
  2. Increases HR and force of contraction of heart
55
Q

Why is a beta-1 agonist (dobutamine) given in cardiogenic shock (pump failure)?

A

This is caused by not enough blood being pumped to maintain blood pressure. The B1 agonist will increase rate and force of contraction.

56
Q

Why is adrenaline administered for anaphylactic shock?

A

In shock blood vessels dilate and therefore blood flow to vital organs cannot be maintained. High concentrations of adrenaline activate alpha-1 receptors causing vasoconstriction.

57
Q

Why is adrenaline administrated in a cardiac arrest?

A
  1. Peripheral vasoconstriction ensures that blood is concentrated to the vital organs - brain and heart
  2. Increases HR and force of contraction of heart
58
Q

Why is a beta-1 agonist (dobutamine) given in cardiogenic shock (pump failure)?

A

This is caused by not enough blood being pumped to maintain blood pressure. The B1 agonist will increase rate and force of contraction.

59
Q

Why would you not give a non-selective B1/B2 antagonist to treat angina/ hypertension/ arrythmias in an asthmatic?

A

Becuase although it would work block B1 receptors in the heart and therefore decrease inotropy and chronotropy, it would also block B2 receptors in the bronchioles and cause bronchioconstriction.

60
Q

Why is salbutamol used as a treatment for asthma?

A

It is a beta-2 agonist - it causes relaxation of bronchiole smooth muscle and thereofre vasodilation of airways.

61
Q

Why are muscarinic agonist, such as pilocarpine, used in the treatment of glaucoma?

A

It activates M3 receptors in the sphincter of the eye which results in contraction of the sphincter muscles and therefore contraction of the pupil. This allows the aqueous humour to drain more and therefore reduces pressure in the eye.

62
Q

What would you give an asthmatic with hypertension instead of a non-selective B1/B2 antagonist?

A

A selective B1 antagoinst. This is cardio-selective and therefore there is less risk of bronchioconstriction.

63
Q

Why is a topical solution of muscarinic antagonist given to examine the eye?

A

It blocks M3 receptors and therefore causes pupil dilation.

ESA2 LKM (45 decks)

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