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BMS03 > Pharmacology Of The Sympathetic NS > Flashcards

Pharmacology Of The Sympathetic NS Flashcards

1
Q

What receptors are present at ganglions?

A

Cholinergic nicotinic

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2
Q

What is the main neurotransmitter of the sympathetic NS?

What are the exceptions?

A

Noradrenaline

Sweat glands - muscarinic (ACh)

Adrenal medulla - nicotinic (ACh)

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3
Q

What are some alpha sympathetic effects?

A

Mydriasis (a1)

Decreased salivation (a1)

Arteriole constriction (a1)

Gluconeogenesis

Smooth muscle relaxation in GI tract

GI tract and bladder sphincter contraction (a1)

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4
Q

What are some beta sympathetic effects?

A

Ciliary muscle relaxation

Increased heart rate via SAN (b1)

Increased heart contractile force (b1)

Bronchodilation (b2)

Gluconeogenesis (b2)

Smooth muscle relaxation in GI tract and bladder (b2)

Skeletal muscle relaxation (b2)

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5
Q

Why do we not target the CNS with drugs?

A

Must pass blood-brain barrier

Likely to have widespread effects

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6
Q

What 5 processes in sympathetic neuroeffector junctions be affected by drugs?

A

Noradrenaline synthesis

Noradrenaline storage

Noradrenaline release

Post-synaptic adrenergic receptor activation

Termination of signalling

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7
Q

What enzyme metabolises unprotected monoamines?

A

Monoamine oxidase (MAO)

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8
Q

What are some examples of monoamines?

A

Noradrenaline

Dopamine

Serotonin

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9
Q

How is noradrenaline taken into vesicles?

A

Vesicular monoamine transporter (VMAT)

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10
Q

What drug inhibits noradrenaline storage?

A

Reserpine

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11
Q

How does reserpine work?

A

Blocks VMAT so noradrenaline isn’t taken up into vesicles

Noradrenaline metabolised by MAO

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12
Q

What reserpine used to treat?

A

Hypertension

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13
Q

What drug is used to inhibit noradrenaline synthesis?

A

a-methyl-tyrosine

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14
Q

How does a-methyl-tyrosine work?

A

Competitive inhibitor against tyrosine

Inhibits tyrosine hydroxylase

Blocks formation of DOPA (from tyrosine)

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15
Q

What is a-methyl-tyrosine used for clinically?

A

Decrease blood pressure in phaechromocytoma (adrenal gland tumour)

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16
Q

How is noradrenaline transported back into the varicosity after release?

A

“Uptake 1” channels

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17
Q

How do drugs inhibit noradrenaline storage?

A

Enter varicosity via “uptake 1” channels

Displace noradrenaline in pre-synaptic vesicles

Noradrenaline metabolised by MAO

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18
Q

What drugs can be used to inhibit noradrenaline release?

A

Guanethidine

Clonodine

Amphetamine

Tyramine

Ephedrine

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19
Q

How is release of noradrenaline usually regulated?

A

After release of noradrenaline, noradrenaline binds to a2 adrenoceptor on pre-synaptic membrane

Inhibits further noradrenaline release by a negative feedback system

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20
Q

What is another name for the a2 adrenoceptor?

A

Autoreceptor

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21
Q

How does clonodine work?

A

a2 adrenoceptor agonist

Mimics effect of high [NA] in synaptic cleft

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22
Q

How do amphetamine/tyramine/ephedrine affect noradrenaline release?

A

Enter varicosity via “uptake 1” channels

Compete with noradrenaline to enter vesicles via VMAT

Noradrenaline leaks into cleft

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23
Q

What is the secondary effect of amphetamine?

A

Inhibits MAO

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24
Q

What type of receptor are adrenoceptors?

A

7TM GPCR

25
Q

What G-protein is coupled to a1 adrenoceptors?

A

Gq

26
Q

What G-protein is coupled to a2 adrenoceptors?

A

Gi

27
Q

What G-protein is coupled to b adrenoceptors?

A

Gs

28
Q

Where are a1 adrenoceptors mainly found?

A

Post-synaptic smooth muscle

29
Q

What does activation of a1 adrenoceptors cause?

A

Activation of PLC, IP3, DAG signalling

Constriction and secretion

30
Q

What does activation of a2 adrenoceptors cause?

A

Inhibition of adenylyl cyclase

Reduced cAMP so less PKA stimulated

Inhibit neurotransmitter release

31
Q

What do a-blockers do?

A

Block sympathetic vasoconstriction tone

To decrease blood pressure

32
Q

What is the important side effect of non-selective a-blockers?

A

Severe reflex tachycardia

33
Q

Why are a2-blockers not used?

A

Too widespread

34
Q

What are a1-blockers used as?

A

Antihypertensive agents (treat hypertension)

35
Q

Give an example of an a1-blocker

A

DOXAZOSIN

Tamsulosin

36
Q

What are some side effects of a1-blockers?

A

Postural hypotension

Diarrhoea

Nasal congestion

37
Q

Where are b1 adrenoceptors mainly found?

A

Cardiac muscle

38
Q

What does activation of b1 adrenoceptors cause?

A

Stimulation of adenylyl cyclase

Increase cAMP

Increase force and rate of heart contractions

39
Q

Where are b2 adrenoceptors mainly found?

A

Smooth and skeletal muscle

Vasculature and airways

40
Q

What does activation of b2 adrenoceptors cause?

A

Stimulate adenylyl cyclase

Increased cAMP

Smooth muscle relaxation (bronchodilation, vasodilation)

(Glycogen mobilisation in liver)

41
Q

What type of drug is labetolol?

A

a1 and b blockers

42
Q

What does labetolol do overall?

A

Reduce arterial blood pressure

43
Q

What is an example of a b-selective blocker?

A

Propanolol

44
Q

What is propanolol used to treat?

A

Disturbances in cardiac rhythm

MI

Angina

45
Q

What are b1-selective blockers often called?

A

Cardio-selective blockers

46
Q

What is an example of a b1-blocker?

A

Atenolol

47
Q

Why are b1-blockers better than b-blockers?

A

Fewer side effects

48
Q

What are some adverse effects of b-blockers?

A

Fatigue (due to decreased cardiac output)

Reduced peripheral blood flow

BRONCHOCONSTRICTION

Increased risk of cardiac failure

Risk of HYPOGLYCAEMIA (patients on insulin therapy)

49
Q

What are b2-agonists used for?

A

Asthma

50
Q

What is an example of a b2-agonist?

A

Salbutamol

51
Q

What does salbutamol do to treat asthma?

A

Promotes bronchodilation

Also induces premature labour

52
Q

What are catecholamines metabolised by?

A

MAO

Catechol-O-methyl transferase (COMT) - in both neuronal and non-neuronal tissue

53
Q

Where is MAO(A) found? (5)

A

CNS

Lung endothelium

Liver

GI tract

Placenta

54
Q

Where is MAO(B) found? (2)

A

CNS

Blood platelets

55
Q

What are some examples of MAO inhibitors?

A

Phenylzine

Moclobemide (A)

Selegiline (B)

56
Q

What is moclobemide selective for?

A

MAO(A)

57
Q

What is selegiline selective for?

A

MAO(B)

58
Q

Why is it dangerous to eat cheese/yogurt or drink wine when taking MAO-inhibitors?

A

Tyramine

Degraded by MAO usually

Tyramine not degraded but converted into noradrenaline

Hypertensive crisis

BMS03 (12 decks)

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