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Noradrenaline Flashcards

1
Q

Cardiovascular effects of sympathetic stimulation

A
  • increased heart rate

- increased force of contraction

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2
Q

Pulmonary effects of sympathetic stimulation

A

bronchodilatation (expansion of bronchial airways)

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3
Q

Gastrointestinal effects

A
  • decreased peristalsis
  • decreased luminal secretions
  • increased vasoconstriction in GI organs
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4
Q

Other effects of sympathetic stimulation

A
  • pupil dilation (mydriasis)
  • glycogenolysis (conversion of glycogen to glucose)
  • lipolysis (breakdown of fats and other lipids by hydrolysis to release fatty acids)
  • renin secretion (enzyme secreted and stored in the kidneys which promotes the production of angiotensin)
  • vasodilatation of skeletal muscles
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5
Q

what type of drug is used to treat asthma?

A

salbutamol, salmeterol
beta2 adrenergic agonist

increased bronchodilation for enhanced gas exchange

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6
Q

type of drug used in premature labour

A

intravenous salbutamol
beta 2 adrenergic agonist

to stimulate uterine relaxation

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7
Q

type of drug used in HTN

A

propranolol
non-selective beta adrenergic antagonist

to decrease blood pressure

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8
Q

type of drug used in angina

A

propranolol
non-selective beta adrenergic antagonist

to decrease heart rate and force of contraction

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9
Q

type of drugs used in benign prostatic hypertrophy

A

prazosin, tamusolin
alpha adrenoreceptor antagonist

to decrease size of prostate gland

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10
Q

where are the sites of drug intervention in the sympathetic nervous system

A

in CNS- drugs would need to penetrate BBB so effects are widespread

in sympathetic ganglion, transmission is similar (ACh mediated) at all autonomic ganglia (sympathetic and parasympathetic), widespread and non-specific effects

BUT at the neuroeffector junction, allows for specific targeting of function e.g. heart, lungs, minimal off-target effects

WANT A DRUG THAT HAS SPECIFIC ACTIONS BUT LIMITED TARGET EFFECTS

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11
Q

what is a ganglion

A

a structure containing a number of cell bodies, typically linked by synapses and often forming a swelling in the nerve fibre

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12
Q

Draw out the synthesis of noradrenaline

A 
tyrosine
    tyrosine hydroxyase
DOPA
    DOPA decarboxylase
dopamine
     dopamine beta hydroxylase 
noradrenaline
     phenylethanolamine- N-methyl transferase
adrenaline
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13
Q

how does alpha-methyl tyrosine interfere with NA synthesis

A

FALSE SUBSTRATE
alpha-methyl tyrosine inhibits the action of tyrosine hydroxylase

blocks formation of DOPA
decrease amount of noradrenaline formed

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14
Q

what are the uses of alpha methyl tyrosine

A
  • decreases blood pressure in pheochromocytoma

benign tumour in adrenal gland causing persistant high blood pressure

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15
Q

side effects of alpha-methyl tyrosine

SPD

A
  • sedation
  • parkinsonism
  • diarrhoea
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16
Q

how does methyldopa intefere with noradrenaline synthesis

A
  • a competitive inhibitor of DOPA decarboxylase, decreases amount of dopamine and noradrenaline synthesis, decreasing sympathetic nervous activity
  • results in the production of alpha-methylnoradrenaline instead
  • lower blood pressure by stimulating inhibitory alpha 2 adrenoceptors in the brainste, decreasing sympathetic nervous activity
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17
Q

how does reserpine intefere with noradrenaline synthesis

A
  • unprotected monoamines (NA, dopamine, serotonin) are metabolised by monoamine oxidase
  • under normal conditions, NA is taken into vesicles via the vesicular monoamine transporter VMAT
  • reserpine blocks VMAT, preventing NA uptake into vesicles leading to its metabolism by MAO to DOPAC- 3,4-dihydroxymandelic acid
  • ## within 24 hours of treatment, the nerve is depleted of NA
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18
Q

what is reserpine used for

A

historical drug
no longer used in the clinic
wide range of effects that leads to depression of the CNS signal

used as antihypertensives

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19
Q

side effects of reserpine

A
  • profound CNS depression
  • diarrhoea
  • nasal congestion
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20
Q

what drugs inhibit NA release

A

guanethidine and debrisoquine

and clonidine

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21
Q

how do guanethidine and debrisoquine inhibit NA release

A
  • after release, NA can be transported back into the varicosity through uptake 1 channels
  • drugs can inhibit NA release by entering the varicosity through these channels and displacing NA in the vesicles
  • this leads to metabolism of NA by MAO and the gradual depletion of NA within the nerve terminal
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22
Q

how does clonidine inhibit NA release?

A

by activation of the alpha 2- adrenergic receptor (AR) on the presynaptic terminal in a negative feedback mechanism

is a alpha- 2 adrenoreceptor specific agonist

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23
Q

uses of clonidine?

A

in hypertension and tachycardia

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24
Q

side effects of clonidine

A
  • postural hypotension
  • headaches
  • diarrhoea
  • fluid retention
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25
what drug promotes NA release
amphetamine, tyramine, ephedrine
26
how does amphetamine promote drug release?
- enter the varicosity through uptake 1 channels NET - drugs can compete with NA to enter the vesicles through the VMAT - drug displaces NA from its storage sites leading to NA leakage into the synaptic gap where it can activate receptors - amphetamine also has secondary effects by inhibiting MAO, increasing the concentration of free NA for release into the synaptic gap
27
what is ephedrine used as?
nasal congestant and bronchodilator
28
what is amphetamine used for?
ADHD
29
side effects of amphetamine, tyramine, ephedrine
- tachycardia - restlesness - insomnia - dry mouth - tolerance - rebound effects
30
what are adrenergic receptors
a class of G protein coupled receptors that are targets of catecholamines
31
what receptors does vascular smooth muscle contain and which drug as the greatest activity?
alpha adrenergic receptors | noradrenaline > adrenaline > isoprenaline
32
what receptors does cardiac smooth muscle contain and which drug has the greatest activity ?
beta adrenergic receptors | isoprenaline > adrenaline > noradrenaline
33
subunits of alpha 1, alpha 2 and beta adrenergic receptors?
A1: a1A, a1B, a1D A2: a2A, a2B, a2C B: B1, B2, B3
34
effect of activating alpha 1 postsynaptic receptors
- vascular smooth muscle contraction ---> vasoconstriction, reduced blood flow, increased blood pressure - relaxation of longitudinal muscle in GI tract - anal sphincter contraction - reduced GI motility ---> constipation - bladder relaxation ---> sphincter contraction- urinary retention - pregnant uterine muscle contraction - radial muscle contraction - increased secretion from salivary glands - increased glycogen mobilisation from the liver - vas deferens circulation (ejaculation)
35
effect of activating alpha 2 presynaptic receptors
- widespread distribution - inhibition of neurotransmitter release negative feedback mechanism
36
effect of activating beta 1 postsynaptic receptors
- predominantly located in the cardiac muscles - increased heart rate - increased force of contraction - increased cAMP production in pacemaker tissue
37
effect of stimulating beta 2 receptors | not at synaptic sites
- relaxation of bronchial smooth muscle (dilation of airways, greater gas exchange, greater absorption of O2 from the blood) - vascular smooth muscle relaxation - skeletal muscle, coronary and hepatic arteriole vasodilation - uterine smooth muscle contraction - glycogen mobilisation in the liver
38
what are sympathomimetics
drugs which mimic the action of endogenous sympathetic nervous agents
39
name some non selective sympathomimetics
noradrenaline and adrenaline
40
action of noradrenaline
potent agonist at alpha 1, alpha 2 receptors moderate agonist at beta 1 weak agonist at beta 2 - emergency treatment of acute hypotension - cardiac arrest
41
action of noradrenaline
- potent agonist at beta 2 and beta 1 receptors - moderate agonist at alpha 1 and 2 receptors - emergency treatment of acute hypotension - cardiac arrest - anaphalyactic shock - given with local anaesthetics
42
name some alpha selective sympathomimetics
phenylephrine and clonidine
43
action of phenylephrine
moderate agonist at alpha 1 receptors - acute hypotension - nasal congestion
44
action of clonidine
- potent agonist at alpha 2 receptors - hypertension - migraine
45
name some beta selective sympathomimetics
isoprenaline salbutamok dobutamine
46
action of isoprenaline
potent agonist at beta 1 and 2 receptors - heart block
47
action of salbutamol
- potent agonist at beta receptors - asthma - premature labour (uterine relaxation)
48
action of dobutamine
potent agonist at beta 2 receptors - cardiogenic shock
49
how do adrenergic receptor antagonists work?
block sympathetic vasoconstrictor tone | resulting in decreased blood pressure
50
name some non selective blockers
phenoxybenzamine (irreversible competitive antagonist) | phentolamine (reversible competitve antagonist can cause severe reflex tachycardia)
51
name some selective alpha blockers
prazosin (in benign prostatic hypertrophy) doxasozin - decreased risk of reflex tachycardia - antihypertensive agents - used in benign prostatic hyperplasia
52
side effects of alpha blockers?
- postural hypotension - nasal congestion - importance - priapism - diarrhoea
53
how do beta blockers work
beta adrenergic antagonists - directly block sympathetic nervous input into the heart - decreased force of contraction - decreased frequency of contraction - decreased vascular tone - leads to decreased cardiac output and decreased blood pressure
54
what drugs are non selective to alpha and beta blockers?
labetalol and carvedilol block both alpha 1 and beta receptors - reduce arterial blood pressure - used in stable congestive heart failure
55
what drugs are beta selective (block both beta 1 and beta 2 receptors)?
- propranolol - timolol - used to treat disturbances in cardiac rhythm, myocardial infarction and angina
56
what drug is beta 1 selective
metoprolol atenolol - used to treat disturbances in cardiac rhythm, myocardial infarction and angina
57
6 adverse effects of beta blockers?
- fatigue reduced cardiac output contributes to decreased muscle perfusion leading to poor response to exercise - reduced peripheral blood flow reynauds syndrome - bronchoconstriction BETA BLOCKERS CONTRAINDICATED IN ASTHMATIC PATIENTS - increased risk of cardiac failure in extreme heart failure, sympathetic tone is important for the maintenance of function - risk of hypoglycaemia - rebound effects
58
Which two enzymes are endogenous and exogenous catecholamines metabolised by?
- monoamine oxidase (within cells bound to surface membrane of mitochondria) - catechol- O- methyl transferase (COMT)- widespread enzyme found in both neuronal and non-neuronal tissues
59
action of MAO
(abundant in noradrenergic nerve terminals but also live in intestinal epithelium) MAO converts catecholamines into their corresponding aldehydes and then by aldehyde dehydrogenase (ADH) to DOMA dihydroxymandelic acid
60
two isoforms of MAO?
MAOa in CNS, pulmonary vascular endothelium, GI tract and placenta MAOb in CNS and platelets
61
examples of MAO inhibitors
phenylzine (irreversible non-selective inhibitor of both isoforms) moclobemide- short acting MAOa selective inhibitor selegiline- irreversible MAOb selective inhibitor --- selective for dopamine and used in PD
62
side effects of MAO-i
- urinary retention - headache - insomnia - postural hypotension - diarrhoea

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