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Hypertension Exam Yr1 > Adrenergic receptors and synapses > Flashcards

Adrenergic receptors and synapses Flashcards

1
Q

What molecules synthesise acetylcholine?

A

Choline + Acetyl coenzyme A
Catalysed by choline acetyltransferase

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2
Q

What molecules synthesise Noradrenaline?

A

Tyrosine + Tyrosine hydroxylase (limiting reagent) —> DOPA

DOPA + DOPA decarboxylase —> Dopamine

Dopamine + Dopamine beta-hydroxylase —> Noradrenaline

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3
Q

How does choline and tyrosine enter the synapses?

A

Na+ transporter (symporter)

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4
Q

What receptors does noradrenaline act on?

A

Adrenergic

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5
Q

What receptors does acetylcholine act on?

A

Muscarinic
Nicotinic

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6
Q

What type of receptors are nicotinic?

A

Ligand gated ion channels

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7
Q

What type of receptors are muscarinic?

A

GPCR

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8
Q

Where are adrenergic receptors found?

A

At the end of the post-ganglionic neuron for the sympathetic nervous system

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9
Q

Where are nicotinic receptors found?

A

At the ganglionic synapse for both the parasympathetic and sympathetic NS

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10
Q

Where are muscarinic receptors found?

A

At the end of the post-ganglionic neuron for the parasympathetic NS

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11
Q

Summarise how vMAT works and what its function is

A

Function = transporting NA into vesicles for transportation

Hydrolysis of ATP = H+ into vesicle
Proton pump = H+ out, NA in

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12
Q

What inhibits vMAT?

A

Reserpine

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13
Q

What is the consequence of reserpine?

A

NA not transported and released
Doesn’t act on adrenergic receptors
Sympathetic affects cant be produced
Decrease HR
Decrease in renin release

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14
Q

What causes Ca2+ to be released

A

Action potential - depolarisation = Ca2+ channels open

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15
Q

What type of channels are Ca2+

A

L-type voltage gated ion channels

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16
Q

Where does Ca2+ get released into?

A

Pre-synaptic terminal

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17
Q

What is the consequence of an increase in Ca2+?

A

Vesicle fusion to membrane and release of neurotransmitter

18
Q

What is the process called for the release of the neurotransmitter?

A

Exocytosis

19
Q

What drug blocks the release of the neurotransmitter?

A

Guanethidine

20
Q

What is the enzyme responsible for breaking down acetylcholine in the synaptic clef?

A

Acetylcholinesterase

21
Q

Why is noradrenaline metabolism important?

A

Terminates noradrenaline

22
Q

What are the 2 enzymes responsible for metabolising NA?

A

MAO - monoamine oxidase
COMT - Catechol-O-methyl transferase

23
Q

What does MAO metabolise NA to?

A

An aldehyde

24
Q

What does COMT metabolise NA to?

A

Carboxylic acid

25
Q

What cofactor does COMT use?

A

SAM - S Adenosyl methionine

26
Q

What type of enzyme is COMT?

A

Mg2+ metalloprotease

27
Q

Why are using MAO or COMT inhibitors not beneficial?

A

Because noradrenaline has a high percentage of reuptake meaning it can be recycled and the process can happen again

28
Q

What do selective seretonin reuptake inhibitors inhibit?

A

Inhibit reuptake of 5-HT

29
Q

How do neurotransmitters pass the synaptic clef?

A

Diffusion

30
Q

What type of receptors are adrenergic receptors?

A

GPCR

31
Q

What are the 3 adrenergic binding sites and what amino acids do each of them have?

A

TM3 - aspartic residue
TM5 - X2 Serine residue
TM6 - Phenylaniline and asparagine

32
Q

What enantiomer must the alcohol group be on a drug for beta 2 agonists?

A

R- enhances activity

33
Q

What type of amines must the drug have for optimal activity?

A

Secondary

34
Q

What gives beta selectivity over alpha?

A

Substituted hydrophobic chain from amine

35
Q

What is the downstream effects of beta2 agonists?

A

G alpha s
Increase cAMP + PKA
PKA deactivates MLCK
MLCK can phosphorylate myosin
no smooth muscle contraction

36
Q

Why is a substitution on the meta carbon important for beta2 agonists?

A

Stops the metabolism of the drug by COMT - wont become inactivated

37
Q

What must the meta substituent be able to do on beta 2 agonists?

A

Hydrogen bond

38
Q

What are the differences between beta 2 agonists and beta1 antagonists?

A

1) perpendicular ring
2) Alcohol group in S enantiomer
3) Short hydrophobic interactions

39
Q

What increases the activity of beta 2 agonists?

A

long hydrophobic chain separated by an ether

40
Q

Summarise the development of beta blockers

A

1) Alpha vs Beta selectivity - hydrophobic chain on amine
2) Agonist vs antagonist - linking group
3) Beta 1 vs beta 2 - hydrogen bonding group in para position

Hypertension Exam Yr1 (10 decks)

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