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pharmacology > Drugs and the Peripheral nervous system L11 > Flashcards

Drugs and the Peripheral nervous system L11 Flashcards

1
Q

where is noradrenaline released

A

released by postganglionic fibres and the sympathetic nervous system

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2
Q

how is noradrenaline synthesised

A

enzyme tyrosine hydroxylase converts tyrosine into DOPA
enzyme DOPA carboxylase converts DOPA to dopamine
enzyme dopamine B-hydroxylase converts dopamine to noradrenaline

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3
Q

how is NA stored

A

in vesicles

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4
Q

how is NA released

A

exocytosis

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5
Q

what types of receptors does NA interact with

A

Alpha or Beta Noradrenergic receptors

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6
Q

how is NA action terminated

A

it is reuptook by transporter and either
1. recycled into vesicles
2. broken down by monoamine oxidase into amines

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7
Q

describe alpha 1,2 noradrenergic receptors
- where are they found
- what type of receptors are they
- what kind of response do they have

A
  1. located on effector tissue of sympathetic nervous system
  2. G protein or metabotropic
  3. slow response
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8
Q

describe beta 1,2 and 3 noradrenergic receptors
- where are they found
- what type of receptors are they
- what kind of response do they have

A
  1. located on effector tissue of sympathetic nervous system
  2. G protein or metabotropic
  3. slow response
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9
Q

what parts of sympathetic nervous system will A1 receptors effect

A
  1. Pupils dilate(radial muscle contracts)
  2. Blood vessels to visceral organs & skin constrict
  3. Brain activity general alertness
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10
Q

what parts of sympathetic nervous system will A2 receptors effect

A

A2 receptors found on presynaptic neurone not effector tissue
- acts as a negative feedback system
- when NA (ACh or other neurotransmitters) binds to them, they inhibit release of further NA dampening down effect of sympathetic NS

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11
Q

what are A2 auto-receptors and heteroreceptors

A
  1. autoreceptors
    - only sensitive to the neurotransmitters or hormones released by the neuron on which the autoreceptor sits
  2. heteroreceptor
    - receptor regulating the synthesis and/or the release of mediators other than its own ligand
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12
Q

what part of the sympathetic nervous system do B1 receptors effect

A
  1. Heart rate increases (and force of contraction)
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13
Q

what part of the sympathetic nervous system do B2 receptors effect

A
  1. Airways in lungs dilate (bronchodilation)
  2. Lens of eye adjust for far vision (ciliary muscle relax)
  3. Blood vessels to limb muscles dilate
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14
Q

what part of the sympathetic nervous system do B3 receptors effect

A
  1. Increase lipolysis (breakdown of triglycerides to fatty acids)
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15
Q

give 5 examples of noradrenergic agonists

A
  1. adrenaline
  2. clonidine
  3. dobutamine
  4. salbutamol
  5. Clenbuterol
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16
Q

describe agonist effects of adrenaline

A

acts on all the noradrenergic receptors
destroyed in gut so has to be injection
- when given locally, it can prolong and isolate local anaesthesia
- mediates vasoconstriction when bound to A1
- when given intramusically, can treat anaphylactic shock
- mediates cardiac stimulation when bound to B1
- mediated bronchiol smooth muscle relaxation when bound to B2

17
Q

describe agonist effects of Clonidine

A

acts on A2 receptors
- it decrease NA release dampen down overall sympathetic system so is used to treat hypertension
- involve a central effect (nucleus tractus solitarius) which results in decrease sympathetic outflow.
- Also used to treat withdrawal symptoms in morphine withdrawal (inhibits central NA release which drives withdrawal symptoms)

18
Q

describe agonist effects of dobutamine

A

acts on B1 receptor
- increased cardiac rate and force so used to treat heart failure

19
Q

describe agonist effects of salbutamol

A

acts on B2 receptors
Used to treat asthma.
beta 2 – mediated bronchiol smooth muscle relaxation:

20
Q

describe agonist effects of Clenbuterol

A

acts on B2 and 3 receptors
B2: bronchodilation- treat asthma
B3: lipolysis/increased metabolism- Increases muscle bulk in athletes/body builders/livestock

21
Q

give examples of Noradrenergic antagonists

A
  1. prazosin
  2. Tamsulson
  3. Propranolol
  4. Atenolol
  5. Timolol
22
Q

describe antagonist effects of prazosin

A

acts on A1 receptors
- A1 – antagonism: vasodilation and decreased vascular resistance treat hypertension
- Side effects: orthostatic or postural hypotension due to some loss in sympathetic reflex

23
Q

describe antagonist effects of Tamsulson

A

acts on A1
- A1 – antagonism: relaxation of smooth muscle in bladder neck, ease of urinary flow treats urination problems in prostate hyperplasia
- Side effects: orthostatic or postural hypotension due to some loss in sympathetic reflex

24
Q

describe antagonist effects of propanol

A

acts on B1 and 2
B1: Used to treat hypertension and angina
Blocking B1 receptors decreases cardiac output and also decreases oxygen demand.
B2: blocking B2 receptors causes bronchoconstriction. Therefore contra-indicative in asthmatics .

25
Q

describe antagonist effects of Atenolol

A

acts on B1
- Used to treat hypertension and angina
Blocking B1 decreases cardiac output and also decreases oxygen demand.

  • Side effect: can cause rebound hypertension/ angina on abrupt withdrawal probably due to B1 receptor supersensitivity
26
Q

describe antagonist effects of Timolol

A

acts on B2 receptors
- Used to treat glaucoma, antagonism of B2– receptors cause ciliary contraction, and decreased intraocular pressure

27
Q

where are Potential sites of drug action on NA neurotransmission

A

Synthesis
Storage
Release
Receptors
Uptake
Metabolism

28
Q

how can synthesis of NA be targeted

A
  1. give a false substrate such as methlyDOPA
    - DOPA carboxylase converts this to MeDA which is converted to MeNA
    - this outcompetes normally NA synthesis. as it uses the same enzymes, less enzyme available to
29
Q

how can synthesis of NA be targeted
what is it used to treat

A
  1. give a false substrate such as methlyDOPA
    - DOPA carboxylase converts this to MeDA which is converted to MeNA
    - this outcompetes normally NA synthesis. as it uses the same enzymes, less enzyme available to synthesise NA so less is made so sympathetic system is inhibited
    - Used in the treatment of hypertension
30
Q

how can storage be targeted
what is it used to treat

A

Reserpine disrupts storage of NA in synaptic vesicles
- Overall decrease in NA neurotransmission
Used to treat hypertension

31
Q

how can release be targeted
what is it used to treat

A

NA release is subject to autoinhibitory control via presynaptic A2 -autoreceptor
clonidine (A2-agonist) causes inhibition of NA release
Overall decrease in NA neurotransmission
Used to treat hypertension

32
Q

how can uptake be targeted
what is it used to treat

A

NA uptake can be blocked by NA reuptake inhibitors
This will prolong the action of NA in the synapse
- desipramine tricyclic antidepressants
- reboxetine selective noradrenaline reuptake inhibitors
- treat depression

33
Q

how can metabolism be targeted
what is it used to treat

A

After reuptake NA is metabolised by the enzymes monoamine oxidase (MAO), and catecholamine transferase (COMT)
- By blocking these enzymes the amount of NA available for release is increased.
- tranylcypramine blocks MAO and allows more NA to be recycled so increases NA neurotransmission.

34
Q

what else does monoamine oxidase (MAO), and catecholamine transferase (COMT) block

A

block the metabolism of dietary amines (e.g. commonly found in cheese, marmite) and amines found in popular cold remedies.
- Accumulation of dietary amines can have a sympathomimetic effect and result in hypertension

pharmacology (13 decks)

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