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Cardiovascular System > Session 4 - CNS and ANS > Flashcards

Session 4 - CNS and ANS Flashcards

1
Q

What are ganglia?

A

-Collections of cell bodies within the PNS

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2
Q

What is a neuro-effector junction?

A

-A synapse between a post-ganglionic neurone and an effector cell

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3
Q

Where do the sympathetic and parasympathetic nervous systems leave the spinal cord?

A
  • Sympathetic from Thoracic and Lumbar regions

- Parasympathetic from Cranial and Sacral regions

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4
Q

Which division of the ANS has long pre-panglionic fibres and short postganglionic fibres?

A

-Parasympathetic

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5
Q

Which division of the ANS has short pre-ganglionic fibres and long post-ganglionic fibres?

A

-Sympathetic

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6
Q

Where are most of the ganglia of the sympathetic nervous system located?

A

-Paravertebral chain

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7
Q

Where are most of the ganglia of the parasympathetic nervous system located?

A

-Close to or within their effector structures

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8
Q

Which fibres and of which divisions have Ach as its neurotransmitter?

A

-Preganglionic fibres of both divisions and post ganglionic of parasympathetic

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9
Q

What is the neurotransmitter of the post-ganglionic fibres of the sympathetic nervous system?

A

-Noradrenaline

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10
Q

What receptors are on post-ganglionic cell bodies?

A

-Nicotinic Ach receptors

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11
Q

What receptors are found on effector cells of the parasympathetic system?

A

-Muscarinic 1,2,3 Ach R

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12
Q

What receptors are found on the effector cells of the sympathetic nervous system?

A

-a and b adrenergic receptors

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13
Q

Which functions are an exception to the sympathetic nervous system?

A

-Perspiration and Ejaculation which use Ach and muscarinic receptors

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14
Q

What type of receptor are muscarinic receptors?

A

-GPCR

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15
Q

What type of receptors are nicotinic receptors?

A

-Fast-acting ion channels

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16
Q

What type of receptors are adrenoreceptors?

A

-GPCR

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17
Q

How does the sympathetic innervation of the adrenal medulla differ from the rest?

A

-Has specialised post-ganglionic neurones called chromaffin cells which secrete adrenaline when stimulated

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18
Q

Whyat effect does the ANS have on the CVS?

A

-Controls HR, force of contraction and vasomotor tone

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19
Q

Through what nerve does parasympathetic input to the heart occur?

A

-Vagus

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20
Q

What neurotransmitter and receptors does the parasympathetic NS use to innervate the heart?

A
  • Ach

- M2 receptors

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21
Q

What effect does the parasympatheric nervous system have on the heart?

A
  • Decrease rate

- Decrease AV node conduction velocity

22
Q

What structures does the sympathetic NS innervate in the heart?

A
  • SA node
  • AV node
  • Myocardium
23
Q

What receptors does the sympathetic nervous system act on in the heart?

A

-B1-adrenoreceptors

24
Q

What effect does the sympathetic nervous system have on contraction?

A
  • Increase rate

- Increased force

25
Q

How does the sympathetic NS increase HR?

A
  • Increases depolarising slope of funny current by stimulating b1-adrenoreceptors
  • b1-adrenoreceptors -> Gas dissociates and activates adenyl cyclase -> this increases cAMP production in the cell which is a cyclic nucleotide
  • cAMP activates more HCN channels increasing the speed of depolarisation, with a resulting increase in hyperpolarisation both increasing the HR
26
Q

How does the parasympathetic NS decrease HR?

A
  • Ach stimulates M2 receptors which have an associated Gai subunit
  • Gai inhibits adenyl cyclase which decreases cAMP -> decreased activation of HCN
27
Q

How are the divisions of the ANS arranged?

A

-Two neurones arranged in series with the pre-gangionic neurone having its cell body in the CNA and the post-ganglionic cell neurone having its body in the PNS

28
Q

The parasympathetic NS increases the conductance of K+ in cels, so why is there an overall decrease in HR?

A

-The decrease in cAMP has a greater effect than the increased hyperpolarisation caused by increased K conduction

29
Q

How does NA (from SNS) increase the force of contraction of the heart?

A

-NA binds to b1-adrenoreceptors
-This activates the GPCR and Gas dissociates from the G protein and activates AC. This increases the production of cAMP with a resultant activation of PKA
-PKA results in the phosphorylation, and thus opening of Ca channels, causing increased entry of Ca during the AP
-NA increases the uptake of Ca into the SR -> more to be released
-NA causes increased sensitivity of contractile machinery to Ca
These cause an increased force of contraction

30
Q

Which type of innervation do most blood vessels get? What is the exception to this?

A
  • Sympathetic

- Erectile tissue which gets parasympathetic

31
Q

What type of adrenoreceptor do most arteries and veins have?

A

-a1-adrenoreceptors

32
Q

Which blood vessels have a1 and b2 adrenoreceptors?

A
  • Coronary vessels

- Skeletal muscle vasculature

33
Q

What is the result of a decreased sympathetic output to blood vessels?

A

-Vasodilatation

34
Q

For those vessels which have B2 and a1-adrenoreceptors, which neurotransmitter does each of them respond to?

A
  • a1-> circulating noradrenaline

- b2->circulating adenaline

35
Q

Why can adrenaline cause vasodilation of some vessels?

A
  • Adrenaline acts on b2-adrenoreceptors in coronary or skeletal musche vessels
  • B2 adrenoreceptor has Gas-type gprotein
  • Gas dissociates and activates adenyl cyclase
  • Increased cAMP production
  • Increased activation of PKA which Increases conduction of K+
  • Inhibits MLCK and causes reduced contraction of smooth muscle as myosin head not phosphorylated
36
Q

How does noradrenaline cause vasoconstriction of vessels?

A
  • NA acts on a1-adrenoreceptor
  • a1 has Gaq gprotein, gaq dissociates and activates PLC
  • PLC cleaves PIP2 into IP3 and DAG
  • IP3 acts on IP3 receptors on SR causing increased calcium release -> contraction can then occur
  • DAG stimulates PKC which inhibits MLCP further influencing contraction as inhibition of MLCP causes increased phosphorylation of MLC
37
Q

What role do local metabolites have in vasodilation?

A
  • Metabolising tissues produce metabolites such as adenosine, H+, K+,increased pCO2
  • This local accumulation has a strong vasodilator effect
38
Q

Why is metabolites causing vasodilation so important?

A

-Allows supply to meet demand ensuring adequate perfusion as highly active tissues will produce lots of metabolites -> high vasodilatation -> increasd bloodflow

39
Q

Where are baroreceptors?

A

-Aorta and coronary sinus

40
Q

What are baroreceptors?

A
  • Nerve endings which are sensitive to stretch detect increases in arterial pressure and relay the information through afferent fibres to the medulla
  • The medulla can then cause bradycardia and vasodilation through efferent pathways to decrease bp
41
Q

What are sympathomimetics?

A

-Drugs which are a and b adrenoreceptor agonists, and thus mimic the effect of the sympathetic nervous system

42
Q

How does the administration of adrenaline restore function in cardiac arrest?

A

-Pharmalogical levels of adrenaline act on a1-adrenoreceptors on vessels causing vasoconstriction and increasing cardiac output

43
Q

-What is dobutamine?

A

-A b1-agonist which is used in cardiogenic shock to increase the force and rate of contraction

44
Q

How does adrenaline treat anaphylactic shock?

A
  • During anaphylaxis there is widespread vasodilation

- Adrenaline acts on a1-adrenoreceptors and causes vasoconstriction through Gaq-> PLC-> IP3-> increased Ca-> contraction

45
Q

Why is salbutamol used to treat asthma?

A
  • Activates b2-adrenoreceptors
  • Gas dissociates and activates adenyl cyclase
  • Increased cAMP-> increased PKA
  • PKA phosphorylates MLCK leading to its inhibition
  • Myosin not phosphorylated
  • Contraction cannot occur
  • Bronchi relax
46
Q

How can a-adrenoreceptor antagonists be used in the treatment of hypertension?

A
  • Antagonist binds to a1-adrenoreceptor and prevents NA binding
  • Prevents vasoconstriction so vasodilatation occurs
  • Lowers pressure
47
Q

Name an anti-hypertensive agent which works as an a-adrenoreceptor antagonist

A

-Prazosin

48
Q

What is propranolol?

A

-Non-selective Breceptor antagonist which slows HR and reduces force of contraction by blocking b1 receptors, but also causes bronchoconstriction by blocking B2 receptors in the bronchi

49
Q

What is atenolol?

A

-Selective b1 receptor antagonist

50
Q

What is pilocarpine?

A

-Muscarinic agonist used in the treatment of glaucoma as it activates constrictor pupillae muscle

51
Q

What is atropine?

A

-Muscurinic antagonist used to increase HR by blocking the parasympathetic innervation of the heart through M2 receptors

Cardiovascular System (19 decks)

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