S5 Autonomic Control of the CVS Flashcards

1
Q

What is the sympathetic and parasympathetic effects on the pupil of the eye? What are the receptors?

A

Sympathetic - dilation (alpha 1)

Parasympathetic - contraction (muscarinic 3)

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2
Q

What is the sympathetic and parasympathetic effects on the airways of the lungs? What are the receptors?

A

Sympathetic - relax (beta 2)

Parasympathetic - contract (muscarinic 3)

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3
Q

What is the sympathetic and parasympathetic effects on the heart? What are the receptors?

A

Sympathetic - increase rate and force of contraction (beta 1)
Parasympathetic - decreases rate (muscarinic 2)

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4
Q

What is the sympathetic effects on the sweat glands? What are the receptors?

A
Localised secretion (alpha 1)
Generalised secretion (muscarinic 3)
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5
Q

What does the autonomic nervous system exert control over?

A
  • smooth muscle
  • exocrine secretion
  • rate and force of contraction in the heart
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6
Q

What does the ANS control in the cardiovascular system?

A
  • heart rate
  • force of contraction of heart
  • peripheral resistance of blood vessels
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7
Q

What doesn’t the ANS do in the cardiovascular system?

A

Doesn’t initiate electrical activity in the heart

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8
Q

What happens if you denervate the heart?

A

It will still beat but at a faster rate (under influence of the vagus (X) nerve)

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9
Q

What neurotransmitter does parasympathetic postganglionic cells release

A

ACh

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10
Q

What receptors does the ACh act on (in the parasympathetic input to the heart)?

A

M2-receptors

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11
Q

What does ACh binding to M2-receptors in the heart cause?

A
  • decreases heart rate (negative chronological effect)

* decrease in AV node conduction velocity

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12
Q

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

A

The 10th cranial nerve - vagus nerve

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13
Q

Where do the postganglionic fibres of the sympathetic nervous system come from?

A

The sympathetic trunk

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14
Q

What does the sympathetic nervous system innervates in the heart?

A
  • SA node
  • AV node
  • myocardium
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15
Q

What does the sympathetic postganglionic fibres release?

A

Noradrenaline

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16
Q

What receptors does the noradrenaline act on (in the sympathetic input to the heart)?

A

Beta-1 adrenoreceptors

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17
Q

What does noradrenaline binding to beta-1 adrenoreceptors in the heart cause?

A
  • increases heart rate (positive chronotropic effect)

* increases force of contraction (positive inotropic effect)

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18
Q

What is the pacemaker of the heart?

A

Cells in the sinoatrial node (SA node) steadily depolarise towards the threshold (pacemaker potential) results in turning on of a slow Na+ conductance (funny current) and Ca2+ channels open

Action potential firing in the SA node sets the rhythm of the heart

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19
Q

What are the effects of the ANS on the pacemaker potential?

A

Sympathetic - increases slope

Parasympathetic - decreases slope

20
Q

How does sympathetic activity speed up the pacemaker potential?

A

Mediated by beta-1 receptors (GPCRs)

Leads to increased cAMP

21
Q

How does parasympathetic activity slow down the pacemaker potential?

A

Mediated by M2 receptors (GPCRs)

Leads to an increase in K+ conductance and a decrease in cAMP

22
Q

How does noradrenaline increase the force of contraction?

A
  1. Noradrenaline acts on beta-1 receptors in myocardium
  2. Increase in cAMP which activates PKA
  3. PKA phosphorylates Ca2+ channels increasing Ca2+ entry during the plateau of the action potential
  4. An increased release of Ca2+ from the sacroplasmic reticulum also occurs
  5. Increased force of contraction (more Ca2+ for each action potential so increased force of contraction)
23
Q

What is the receptor that most arteries and veins have? What other receptor for coronary and skeletal muscle vasculature also have?

A

Alpha-1 adrenoreceptors

Beta-2 receptors

24
Q

Do most vessels receive sympathetic or parasympathetic innervation?

A

Sympathetic

Erectile tissue have parasympathetic innervation

25
Q

What is the vasomotor tone?

A

The “normal”/basal level which can become vasodilation or vasoconstriction based on a decrease or increase in sympathetic output

26
Q

As well as alpha-1 adrenoceptors, some blood vessels (e.g. skeletal muscle, myocardium, liver) can also have what type of receptor?

A

Beta-2 adrenoceptors

27
Q

Which receptor does noradrenaline from the sympathetic nervous system act on? What is the response?

A

Alpha-1 adrenoceptors causing vasoconstriction

28
Q

Which receptor does (circulating) adrenaline act on? What is the response?

A

Beta-2 adrenoceptors causing vasodilation

29
Q

Which receptor does an increase in adrenaline act on? What is the response? When does this happen?

A

Alpha-1 adrenoceptors casing vasoconstriction

Pharmacologically e.g. adrenaline given in anaphylactic shock

30
Q

Does circulating adrenaline have a higher affinity for beta-2 or alpha-1 adrenoceptors?

A

Beta-2 adrenoceptors

However at higher concentrations it will also activate alpha-1 adrenoceptors

31
Q

Where is circulating adrenaline released from?

A

Adrenal glands

32
Q

What are the effects of beta-2 and alpha-1 adrenoceptors on vascular smooth muscle?

A
  • beta-2 adrenoceptors cause vasodilation (increased cAMP, PKA activated, K+ channels open (decreased depolarisation), inhibits MLCK (so can’t activate myosin light chain), relaxation of smooth muscle)
  • alpha-1 adreoceptors caused vasoconstriction (increased IP3, increase in intracellular Ca2+ conc from stores and influx of extracellular Ca2+, contraction of smooth muscle)
33
Q

What effect does local increases in metabolites on vascular changes?

A

Strong vasodilator effect (more important in ensuring adequate perfusion of skeletal and coronary muscle than activation of beta-2 adrenoceptors)

34
Q

What are some examples of metabolites?

A

Adenosine, K+, H+, increased pCO2

Produced from active tissues

35
Q

How is the CVS controlled overall?

A

Changes in state are communicated to the brain via afferent nerves e.g. baroreceptors and atrial receptors which leads to altered activity of efferent nerves

36
Q

Where in the CVS are baroreceptors and atrial receptors found?

A

Baroreceptors - high pressure side of system e.g. arterial system

Atrial receptors - low pressure side of system

37
Q

Where can be baroreceptors be found in the CVS?

A

Carotid sinus and aortic arch

38
Q

What do baroreceptors detect?

A

Increases blood pressure based off of “stretch”

39
Q

What is the baroreceptor reflex?

A
  1. High mean arterial pressure (MAP)
  2. Detected by baroreceptors
  3. Afferent pathway communicates this to the coordinating centre (medulla)
  4. Efferent pathways communicates this to the effectors (e.g. heart and vessels)
  5. Bradycardia and vasodilation occur
40
Q

Is the baroreceptor reflex useful short or long term? Why?

A

Short term

Baroreceptors can reset to higher levels with persistent increases in blood pressure

41
Q

What are sympathomimetics?

A

Alpha and beta adrenoceptor agonists

42
Q

What are cholinergics?

A

Muscarinic agonists and antagonists

43
Q

What are some cardiovascular uses of sympathomimetics? What is one other use of sympathomimetics?

A
  • administering adrenaline to restore function in cardiac arrest
  • dobutamine (beta-2 agonist) given in cardiogenic shock (pump failure)
  • adrenaline administered for anaphylactic shock
  • salbutamol (beta-2 agonist) treats asthma (bronchodilation)
44
Q

How does giving adrenaline for anaphylactic shock work?

A

Increase adrenaline levels above circulating levels to activate alpha-1 receptors to overcome beta-2 receptors to cause vasoconstriction to increase blood pressure (as beta-2 cause vasodilation)

45
Q

What are adrenoreceptor antagonists (alpha and beta)?

A
  • alpha-adrenoreceptor antagonists - prazosin (alpha-1 antagonist) inhibits noradrenaline action on vascular smooth muscle alpha-1 receptors (vasodilation)
  • beta-adrenoreceptor antagonists - propranolol (non-selective beta-1/beta-2 antagonist) slows heart rate and reduces force of contraction (beta-1) and acts on bronchiole smooth muscle causing bronchoconstriction (beta-2)
  • atenolol (cardio-selective beta-1 antagonist) which has less risk of bronchoconstriction
46
Q

What is an example of a muscarinic agonist?

A

Pilocarpine - treatment for glaucoma - activates constrictor pupillae muscle

47
Q

What is an example of a muscarinic antagonist?

A

Atropine/tropicamide- increase heart rate, cause bronchodilation - used to dilate pupils for examination of the eye