CVS 4.2 - Autonomic Nervous System in the CVS Flashcards

1
Q

Describe the organisation of the sympathetic nervous system

A
  • Origin = Thoracolumbar (T1-L2/L3)

- Synapse at paravertebral chain (heart, lungs etc) or prevertebral ganglia (to liver, GI tract etc)

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2
Q

Describe the length of the ganglia in the SNS

A
  • Preganglionic = Short

- Postganglionic = Long

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3
Q

What types of ganglia are in the SNS?

A
  • Preganglionic = Cholinergic (have nicotinic receptors)

- Postganglionic = Noradrenergic (except sweat with is Ach - muscarinic receptors)

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4
Q

Name some sympathetic receptors to Adrenaline and Noradrenaline. Which is significant to CVS?

A
  • Gq alpha 1 - Pupil dilation and localised secretion
  • Gs beta 1 (SIGNIFICANT TO CVS) - Increase heart rate and force of contraction
  • Gs beta 2 - Relaxation of airways
  • Gq m1/3 - Generalised secretion
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5
Q

Where do sympathetic post ganglionic fibres synapse on the heart?

A
  • Sinoatrial node
  • Atrioventricular node
  • Myocardium (force of contraction)
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6
Q

What happens when Noradrenaline activates Beta-1 receptors in the heart?

A
  • Increased heart rate (positive chronotropic effect)

- Increased force of contraction (positive inotropic effect)

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7
Q

How is heart rate increased by the SNS?

A
  • Noradrenaline binds to Beta-1 receptors coupled to Gs proteins on SAN
  • Stimulates adenylyl cyclase which increases cAMP (cyclic nucleotide for HCN channels)
  • Increased cAMP = Increased open HCN channels
  • Faster depolarisation
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8
Q

How is force of contraction increased by the SNS?

A
  • Noradrenaline binds to Beta-1 receptors coupled to Gs proteins in myocardium
  • Stimulates adenylyl cyclase which increases cAMP
  • Activates PKA so Ca2+ channels are phosphorylated
  • Increases Ca2+ entry into myocytes
  • Increased CICR and sensitivity of contractile machinery
  • Increased uptake of Ca2+ into SR which decreases duration of contraction
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9
Q

Describe the innervation of vasculature

A

Sympathetic except erectile tissue

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10
Q

Which receptors are present in arteries and veins

A

Alpha-1 adrenoreptors (noradrenaline)

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11
Q

Which receptors are present in coronary and skeletal muscle?

A

Beta-1 and beta-2 receptors

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12
Q

Why is having only beta-2 receptors in coronary muscle significant?

A
  • Needs a continuously high blood flow so unable to constrict
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13
Q

How is vasoconstriction caused by SNS?

A
  • Binding of Noradrenaline to alpha-1 receptors stimulates production of IP3
  • Increases intracellular Ca2+ from stores and via influx (IP3 gated ion channel)
  • Binds to calmodulin which activates MLCK
  • Myosin light chain is phosphorylated = CONTRACTION
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14
Q

How is vasodilation caused by SNS?

A
  • Noradrenaline binds to beta-2 receptors which stimulates adenylyl cyclase
  • Increased cAMP production stimulates PKA
  • Opens K+ channels (hyperpolarisation) and inhibits MLCK = DILATION
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15
Q

Describe the organisation of the parasympathetic nervous system

A
  • Origin = Craniosacral - medulla (cranial nerves - eye, salivary glands etc.) or sacral region (S2-S4 - bladder, genitalia)
  • Synapse close to target tissue
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16
Q

Describe the length of ganglia in the PNS

A
  • Preganglionic = long

- Postganglionic = short

17
Q

What types of ganglia are in the PNS?

A
  • Preganglionic = cholinergic (nicotinic receptors that have integral ion channels)
  • Postganglionic = cholinergic (muscarinic that are G protein coupled)
18
Q

Name some parasympathetic receptors to Acetylchline. Which is significant to CVS?

A
  • Gq m1/3 - Stimulates phospholipase C - Constriction of pupil and contraction of airways
  • Gi m2/4 - Inhibits adenylyl cyclase - Decreases heart rate (SIGNIFICANT TO CNS)
19
Q

Where does the vagus nerve of the PNS synapse on the heart?

A
  • Epicardial surface
  • Walls of SAN and AVN
  • Some in ventricles
20
Q

How is heart rate reduced by the PNS?

A
  • Acetylcholine binds to m2 receptors coupled to Gi proteins in the SAN
  • Inhibits adenylyl cyclase which decreases cAMP levels so open HCN channels are decreased
  • Also increases K+ conductance so RMP is further from threshold
  • Reduces pacemaker potential therefore slower depolarisation
21
Q

What is the function of the ANS?

A

Regulation of physiological processes

22
Q

Give two details about the SNS

A
  • Can be independently regulated

- Dominant under stress

23
Q

What does the SNS control?

A
  • Smooth muscle
  • Exocrine secretion
  • Heart rate
  • Force of contraction of heart
24
Q

When is the PNS dominant?

A

Basal states

25
What does the PNS control?
- Sexual Arousal - Lacrimation - Urination - Digestion - Defecation
26
What are Sympathomimetics?
- Drugs that mimic the SNS - Alpha adrenoreceptor agonists - Beta adrenoreceptor agonists
27
Describe the use of adrenaline in cardiac arrest
- Beta adrenoreceptor agonist (causes vasodilation) - Alpha adrenoreceptor agonist in peripheries (restores blood pressure and returns blood to the heart) (Dose is higher than physiological levels so both are activated)
28
Describe the use of Dobutamine in cardiogenic shock
- Beta-1 agonist | - Increases heart rate and force of contraction to bring pump system back to normal
29
Describe the use of Salbutamol for asthma
- Beta-2 agonist | - Relaxation of airways
30
Describe the use of Propanolol for treatment of tremors/angina. Why is it inappropriate to use for asthmatics?
- Non selective antagonist for Beta-1 and Beta-2 adrenoreceptors - Decreases heart rate and force of contraction but causes bronchoconstriction (so not appropriate for asthmatics)
31
Why is Atenolol more appropriate to use that Propanolol when treating asthmatics?
- Cardioselective for Beta-1 adrenoreceptors | - Doesn't cause bronchoconstriction
32
Why is Prazosin used as an antihypertensive?
- Alpha-1 antagonist | - Blocks alpha one so prevents vasoconstriction
33
Give two example of cholinergic drugs, their effects and uses
- Pilocarpine (Agonist) = Pupil constriction by activating constrictor pupillae muscles (Glaucoma treatment) - Atropine (Antagonist) Antagonist = Pupil dilation (eye examinations)