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Phys Pharm I > adrenoceptor pharmacology > Flashcards

adrenoceptor pharmacology Flashcards

1
Q

what is adrenaline and where is it released from?

A

a hormone released from chromaffin cells in the adrenal medulla

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2
Q

what is noradrenaline and where is it released from?

A

a neurotransmitter released by sympathetic nerve terminals in the central and autonomic nervous system

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3
Q

what is the significance of the pons?

A

contains more noradrenergic cell bodies than any other place in the nervous system

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4
Q

where do most noradrenergic projections originate? from?

A

the locus coerulus

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5
Q

outline how noradrenaline mediates post-ganglionic actions in the ANS

A

chromaffin cells receive a sympathetic pre-ganglionic innervation -> acetylcholine is released -> chromaffin cell depolarises -> adrenaline is released into the blood stream

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6
Q

what is a varicosity?

A

a region of the axon where neurotransmitter can be made and released, each contains everything required for synthesis and re-uptake of neurotransmitter

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7
Q

what is the role of the varicosity?

A

to mediate the level of NA in the body by synthesis and recycling existing NA depending on signal received from pre-junctional adrenoceptors

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8
Q

what is the role of pre-junctional adrenoceptors?

A

sensing how much NA is present outside the varicosity

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9
Q

other than NA regulation, what else is the noradrenergic varicosity responsible for?

A

co-release of mediators such as ATP and neuropeptide 7

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10
Q

what is the role of the sodium pump on the noradrenergic varicosity?

A

removes excess NA

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11
Q

outline the steps of synthesis of adrenaline

A

tyrosine hydroxylase converts dietary tyrosine to DOPA -> DOPA decarboxylase converts DOPA to dopamine -> dopamine-B-hydroxylase converts dopamine to noradrenaline -> phenylethanolamine N-methyltransferase converts noradrenaline to adrenaline

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12
Q

what are the stages in adrenergic transmission?

A

synthesis, storage/compartmentalisation, release, signal transmission, signal termination

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13
Q

what does the dopamine/noradrenaline transporter on noradrenergic terminal vesicles do?

A

uses transvesicular proton gradient as a driving force to allow accumulation of noradrenaline at very high concentrations (0.5-1M) inside vesicles

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14
Q

how does NA regulate its own release?

A

acts on pre-synaptic B2 receptors, receiving autoinhibitory feedback

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15
Q

what triggers NA release?

A

depolarisation of the nerve terminal. action potential causes voltage-gated calcium channels to open, allowing calcium flux into the vesicle and causes vesicle fusion

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16
Q

how is noradrenaline removed from the synaptic cleft?

A

cleared by a high affinity uptake mechanism ‘uptake 1/NET’, NA evading this mechanism is cleared by uptake 2

17
Q

how is noradrenaline metabolised?

A

by monoamine oxidase (MAO) catechol O-methyltransferase (COMT) or aldehyde dehydrogenase/reductase

18
Q

how much noradrenaline is repackaged and metabolised?

A

90% repackaged, 10% metabolised

19
Q

what are MAO and COMT used for therapeutically?

A

treatment of parkinson’s disease by bolstering dopamine levels in the brain

20
Q

what are MAO and COMT inhibitors used for therapeutically?

A

treatment of parkinson’s disease by bolstering dopamine levels in the brain

21
Q

what is the primary ligand of the sympathetic ANS at the neuroeffector junction?

A

noradrenaline

22
Q

what is the functional importance of packaging of noradrenaline inside varicosities?

A

it allows the autonomic nervous system to control activity of a vast area of smooth muscle in a highly coordinated way

23
Q

how does a-methylnoradrenaline differ from noradrenaline?

A

1- more resistant to metabolism by MAO/COMT compared to noradrenaline (accumulates over time)
2- a-methylnoradrenaline is a selective agonist at some adrenoceptors

24
Q

what is a-methyltyrosine?

A

an analogue of tyrosine that competitively inhibits tyrosine hydroxylase, this blocks de novo synthesis of noradrenaline

25
Q

what is a-methylDOPA?

A

an analogue of DOPA, which is converted to a-methyldopamine by dopa-decarboxylase and a-methylnoradrenaline by dopamine-B-hydroxylase

26
Q

what kind of drug is methylphenidate? how does it work?

A

indirectly acting sympathomimetic amine - a false substrate for NET. works by accumulating in noradrenergic varicosities to cause release of noradrenaline from the terminal

27
Q

what is a NET inhibitor?

A

a drug that inhibits the reuptake of noradrenaline e.g. cocaine

28
Q

what did studies of adrenoceptor structure in the 1980s find?

A

all adrenoceptors have 7TM topology, the ligand forms a variety of non-covalent interactions on the binding site, allowing the receptor to change conformation

29
Q

how are beta adrenoceptors coupled?

A

positively to adenylyl cyclase via Gs proteins

30
Q

which adrenoceptor subtypes couple negatively to adenylyl cyclase?

A

a2, a2b, a2c.

via Gi/o proteins

31
Q

which adrenoceptor subtypes couple positively to phospholipase C?

A

a1a, a1b, a1d

32
Q

give an example of where adrenoceptors cause different responses to the same ligand in different tissues

A

in the heart, B1-adrenoceptors mediate sympathetic/noradrenaline positive inotropic and chronotropic effects.
in the airways, B2-adrenoceptors mediate bronchodilatory effects

33
Q

give examples of where adrenoceptor agonists are used therapeutically

A

in the CV system e.g. dobutamine is used for acute management of heart failure, cardiac arrest and heart block
in the respiratory system - salbutamol, terbutaline are used for asthma/copd

34
Q

give examples of where adrenoceptor antagonists are used therapeutically

A

a-adrenoceptor antagonists - prazosin, doxazosin for mild hypertension
b-adrenoceptor antagonists - propranolol, atenolol, used to treat hypertension, angina pectoris, cardiac dysrthymias

35
Q

how are the actions of noradrenaline terminated?

A

uptake by a pre-synaptic Na dependent transporter

Phys Pharm I (11 decks)

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