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ESA 2 > CVS 4.2 - Autonomic Nervous System in the CVS > Flashcards

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
Q

What does the PNS control?

A
  • Sexual Arousal
  • Lacrimation
  • Urination
  • Digestion
  • Defecation
26
Q

What are Sympathomimetics?

A
  • Drugs that mimic the SNS
  • Alpha adrenoreceptor agonists
  • Beta adrenoreceptor agonists
27
Q

Describe the use of adrenaline in cardiac arrest

A
  • 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
Q

Describe the use of Dobutamine in cardiogenic shock

A
  • Beta-1 agonist

- Increases heart rate and force of contraction to bring pump system back to normal

29
Q

Describe the use of Salbutamol for asthma

A
  • Beta-2 agonist

- Relaxation of airways

30
Q

Describe the use of Propanolol for treatment of tremors/angina. Why is it inappropriate to use for asthmatics?

A
  • 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
Q

Why is Atenolol more appropriate to use that Propanolol when treating asthmatics?

A
  • Cardioselective for Beta-1 adrenoreceptors

- Doesn’t cause bronchoconstriction

32
Q

Why is Prazosin used as an antihypertensive?

A
  • Alpha-1 antagonist

- Blocks alpha one so prevents vasoconstriction

33
Q

Give two example of cholinergic drugs, their effects and uses

A
  • Pilocarpine (Agonist) = Pupil constriction by activating constrictor pupillae muscles (Glaucoma treatment)
  • Atropine (Antagonist) Antagonist = Pupil dilation (eye examinations)

ESA 2 (63 decks)

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