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PA20016 > Cardiovascular, renal and peripheral nervous system 2 > Flashcards

Cardiovascular, renal and peripheral nervous system 2 Flashcards

1
Q

What are the other names for adrenaline and noradrenaline?

A

Epinephrine and norepinephrine.

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2
Q

What fibres release noradrenaline?

A

Most postsynpatic sympathetic fibres.

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3
Q

Where are cell bodies in sympathetic fibres?

A

Sympathetic ganglion - they send axons ending in varicosities.

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4
Q

What are varicosities?

A

End of axons that are bulbous enlargements.

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5
Q

Where do initial stages of synthesis of noradrenaline occur?

A

In the cytoplasm.

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6
Q

Where do the final stages of synthesis of noradrenaline occur?

A

On the membrane of the synaptic vesicle.

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7
Q

What is the precursor molecule for noradrenaline?

A

The amino acid L-tyrosine - which is also the precursor molecule for dopamine.

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8
Q

How does noradrenaline regulate its production?

A

Via a negative feedback process on the initial step of synthesis.

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9
Q

Where does production of enzymes involved in transmitter synthesis occur?

A

In the cell body.

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10
Q

Where are transmitters made?

A

At the nerve ending.

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11
Q

What does the negative feedback aspect of NA synthesis prevent?

A

The formation of the precursor DOPA.

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12
Q

What is the first enzyme involved in the formation of noradrenaline?

A

Tyrosine hydroxylase - catalyses the formation of DOPA from L-tyrosine.

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13
Q

What is the formation of DOPA inhibited by?

A

Alpha-methyl-p-tyrosine - Metirosine.

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14
Q

What clinical use can Metirosine be involved in?

A

Phaeochromocytoma - tumour of adrenal gland tissue.

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15
Q

What is the second stage of synthesis of noradrenaline and what enzyme catalyses it?

A

DOPA to dopamine by DOPA decarboxylase.

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16
Q

What inhibits the formation of dopamine from DOPA?

A

Carbidopa.

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17
Q

What drug is used in Parkinson’s treatment?

A

Carbidopa along with levodopa to prevent peripheral effects.

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18
Q

How are the drugs used to treat Parkinson’s successful?

A

Carbidopa cannot cross the blood brain barrier so levodopa metabolism can continue in the brain but not in the periphery - reduced side effects.

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19
Q

What are the side effects of increased L-DOPA in the periphery?

A

High blood pressure and racing heart.

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20
Q

How is noradrenaline released?

A

There is depolarisation of nerve endings that opens calcium channels and leads to vesicle exocytosis.

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21
Q

How does the negative feedback of noradrenaline release occur?

A

Noradrenaline activates presynaptic receptors that inhibit adenylyl cyclase which prevents calcium channel opening and limits the further release of noradrenaline.

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22
Q

What is the presynaptic receptor that is coupled with adenylyl cyclase?

A

The alpha 2 receptor.

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23
Q

What is methyldopa?

A

A drug that inhibits the release of noradrenaline. It is an alpha 2 agonist that is a false precursor molecule.

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24
Q

What is methyldopa metabolised to?

A

Methyl-NA.

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25
Q

What is methyldopa used to treat?

A

Pregnancy-induced hypertension.

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26
Q

What else does methyldopa inhibit?

A

DOPA decarboxylase - like carbidopa.

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27
Q

Where is the free concentration of noradrenaline in the neuron cytoplasm low?

A

Monoamine oxidase - MAO.

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28
Q

How is noradrenaline taken up into vesicles?

A

Vesicular monoamine transporter - VMAT.

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29
Q

What is co-released with noradrenaline?

A

ATP - it is a co-transmitter.

30
Q

What is the purpose of the co-transmitter of noradrenaline?

A

ATP has an opposite charge and helps prevent leak from vesicles.

31
Q

What removes noradrenaline from the synaptic cleft?

A

Neuronal epinephrine transporter (NET).

32
Q

Where is NET found?

A

The presynaptic nerve terminals - it actively transports NA back into the nerve varicosities.

33
Q

What repackages noradrenaline back into vesicles?

A

VMAT.

34
Q

What is another way that noradrenaline can be removed from the synaptic cleft?

A

Extraneuronal monoamine transporter - EMT.

35
Q

How does EMT work?

A

It actively transports catecholamines into the postsynaptic cell, which are then metabolised by catechol o-methyl transferase - COMT.

36
Q

What is another drug that inhibits the release of noradrenaline?

A

Guanethidine.

37
Q

How does guanethidine work?

A

It is a substrate for NET and VMAT. It accumulates in vesicles and stabilises them and displaces NA slowly (taken up instead of NA). Free NA is metabolised by MAO. High doses destroys the neuron.

38
Q

What is the overall effect of guanethidine?

A

It blocks adrenergic neurons.

39
Q

What drug causes the depletion of NA?

A

Reserpine.

40
Q

How does reserpine work?

A

It inhibits VMAT so NA cannot be transported into vesicles. Cytoplasmic NA is still metabolised by MAO so vesicular levels fall.

41
Q

What can reserpine be used as ?

A

An antihypertensive.

42
Q

What are some of the side effects of reserpine?

A

Depression and Parkinsonism - similar side effects to methyldopa.

43
Q

What are some unwanted effects of inhibiting NA synthesis and release?

A

Anti-sympathetic effects - hypotension, bradycardia, digestive disorders, nasal congesion and sexual dysfunction.

44
Q

What are some central side effects associated with inhibiting NA synthesis/release?

A

Sedation, mood disturbances.

45
Q

What are the two substances that can terminate noradrenaline?

A

Monoamine oxidase (MAO) and catechol-o methyl transferase.

46
Q

Where is MAO found?

A

Mainly in neurones but also in the liver and GI tract.

47
Q

What does MAO do?

A

Converts noradrenaline to DOMA.

48
Q

Where is catechol-o methyl transferase found?

A

In neuronal and non-neuronal tissue.

49
Q

What else does catechol-o methyl transferase do?

A

It metabolises DOMA produced from MAO.

50
Q

What does alpha-methyltyrosine do?

A

Stop conversion of tyrosine to NA.

51
Q

What do MAO inhibitors do?

A

Stop metabolites being converted back to NA.

52
Q

What does reserpine do?

A

Prevent the formation of NA.

53
Q

What is the active agent in the adrenal glands?

A

Adrenaline.

54
Q

What is the sympathetic neurotransmitter involved in the adrenal glands?

A

Noradrenaline.

55
Q

What is the difference between alpha and beta adrenoceptors?

A

Alpha - vasoconstrictor, beta - vasodilator that causes increased heart rate and force.

56
Q

What are the further subdivisions of alpha and beta adrenoceptors?

A

Alpha 1 and 2, beta 1 2 and 3.

57
Q

How do different receptor subtypes cause different effects?

A

Coupling to different second messenger systems.

58
Q

How does one drug have different effects on different tissues?

A

Different receptors present in the different tissue.

59
Q

What is the function of the alpha 1 receptor?

A

Constricts most smooth muscle, except in the GI tract where it relaxes it.

60
Q

What is the effect of the alpha 2 receptor?

A

It causes presynaptic inhibition of neurotransmitter release - sympathetic and parasymapthetic neurons.

61
Q

What is the effect of the beta 1 receptor?

A

It increases heart rate and force of contraction.

62
Q

What is the effect of the beta 2 receptor?

A

It dilates/relaxes smooth muscle - there is increased NA release from sympathetic nerves.

63
Q

What effect does the beta 3 receptor have?

A

It causes thermogenesis (production of heat) in skeletal muscle.

64
Q

What is the selectivity of adrenoceptors for adrenaline and noradrenaline?

A

Relatively unseletive - similar affinity.

65
Q

What receptors does NA activate?

A

Alpha and beta adrenoceptors.

66
Q

What receptors does adrenaline activate?

A

Alpha and beta adrenoceptors.

67
Q

What receptors is NA more potent at?

A

Alpha1 and beta1.

68
Q

What receptors is adrenaline more potent at?

A

Beta2 and alpha2.

69
Q

What are beta receptors coupled with?

A

Gs - stimulates adenylyl cyclase.

70
Q

What are alpha1 receptors coupled to?

A

Phospholipase C .

71
Q

What do alpha2 receptors do?

A

Inhibit adenylyl cyclase, decrease release of adrenaline and ACh.

72
Q

What are agonists?

A

Agents that bind to a receptor and elicit a response.

PA20016 (10 decks)

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