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NAS > Wk9 Autonomic Pharmacology > Flashcards

Wk9 Autonomic Pharmacology Flashcards

1
Q

Nicotinic cholinergic receptor

A
  • depolarisation and firing up of APs when this occurs
  • ligand gates
  • they all have different alpha subunits
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2
Q

What is hexamethonium?

A

• Selective antagonist for the neuronal sub-type of nicotinic receptor
• Not competitive
• Blocks all the effects of autonomic stimulation - blocks ion channel - na+ cant move through, but ACh still binds
• One of the methonium derivatives (like decamethonium)
- sympathetic and parasympathetic stopped - opposite and so not effective
- first drug to lower BP
- injection

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3
Q

What are muscarinic receptors?

A

Parasympathetic Postganglionic Transmission:
ACh is released onto Muscarinic Receptors:
•7 transmembrane segments. (M1, m2, m3, m4, m5)
•5 subtypes, of which the first 3 (M1-3) are particularly important in the periphery - G-protein coupled receptors
- conducts muscle
- mediate transmission from parasympathetic post ganglionic neurones onto the tissues

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4
Q

What are muscarinic agonists?

A

Such drugs are “Parasympathomimetic drugs” because exposure mimics the effects of parasympathetic nervous system activation

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5
Q

Effects of parasympathomimetics

A

Cardiovascular - decreased heart rate
Smooth muscle - contracts, although vascular smooth muscle dilates via endothelium (EDRF = NO) endothelium derived relaxing factor
Exocrine glands - secrete - sweating, lacrimation, salivation,
bronchial secretion

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6
Q

What is muscarine poisoning?

A

• Muscarinicagonist
• Source:many mushrooms
• Adverse Effects:
– bradycardia, vasodilation (secondary to NO), leading to falling BP
– increased gut motility (colicky pain), bronchoconstriction, pupillary constriction (miosis).
– Salivation, lacrimation, airway secretions
• Treatment:
– muscarinic antagonist (atropine).

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7
Q

What is pilocarpine?

A

• Use: to treat glaucoma (some forms)
• Route of administration: topical to the
eye
• Action: On M3 receptors on ciliary muscle, improving aqueous humor drainage, dropping intraocular pressure.
Improves drainage in anterior component of eye

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8
Q

What are muscarinic antagonists?

A

5 subclasses (M1-5) - 3 are important peripherally

Less specific antagonists: atropine (from Belladonna), hyoscine, cyclopentolate.

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9
Q

M1

A

Stomach, salivary glands

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10
Q

M2

A

Cardiac

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11
Q

M3

A

Smooth muscle

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12
Q

Clinical Uses of Antimuscarinic Drugs

A
  • Asthma (ipratropium)
  • To treat bradycardia (atropine)
  • During operations: decrease secretions, decrease AChEI side-effects (atropine)
  • To dilate pupils (tropicamide)
  • Urinary incontinence (oxybutynin or tolterodine)
  • Motion sickness (hyoscine)
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13
Q

Pharmacology of Adrenergic Transmission: Overview

A
  1. α-adrenoceptor agonists and antagonists
  2. β-adrenoceptor agonist and antagonists
  3. Noradnrenaline transporter blockers
  4. Monoamine oxidase inhibitors
  5. Indirectly acting sympathomimetic amines
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14
Q

Adrenoreceptors

A

• 5 main sub-types
–a1
• contract smooth muscle (eg. vasoconstriction)
–a2
• Pre-synaptic auto-inhibition, direct vasoconstriction, central inhibition of sympathetic outflow
–b1
• increase heart rate and contractility
–b2
• relax smooth muscle (eg. bronchodilation,
vasodilation)
–b3
• Relax smooth muscle (bladder); simulate lipolysis

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15
Q

Main uses of a-adrenoceptor receptor agonists

A

• vasoconstrictors with local anaesthetics (mainly a1)
– adrenaline, noradrenaline
• nasal decongestants (mainly a1)
– phenylephrine
• hypertension (central a2)
• Facial erythema in rosacea
– Brimonidine1 (a2; direct vasoconstriction)

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16
Q

a1 Adrenoceptors: coupled to phospholipase C-ß

A

Noradrenaline binds to receptor activating an accessory G protein bound to an intracellulaire loop on the receptor

Gq protein dissociates

Phospholipase C activated, releasing signalling molecules

IP3 receptor - sarcoplasmic reticulum increases release of Ca2+ and contraction stimulated

17
Q

α1- adrenoceptor

A

Gq
PLC
Increased IP3/DAG

18
Q

α2- adrenoceptor

A

Gi
Decreased AC
Decreased cAMP

19
Q

β- adrenoceptor (all)

A

Gs
Increased AC
Increased cAMP

20
Q

M1, M3

A

Gq
PLC
Increased PI3/DAG

21
Q

M2

A

Gi
Decreased Ac
Decreased cAMP

22
Q

Main uses of a-adrenoceptor antagonists

A
  • Hypertension (a1; doxazosin)

* Benign prostatic hyperplasia – tamsulosin (a1)

23
Q

Main uses of b-adrenoceptor agonists

A 
• Cardiogenic shock (b1) 
– adrenaline, dobutamine
• Anaphylactic shock (a/b) 
– adrenaline (increase cardiac output)
• Asthma (b2)
– salbutamol
– also delay of premature labour
e.g. metoprolol (b1)
• angina, cardiac arrhythmias
• hypertension
• anxiety states
• (chronic) heart failure (give the heart a
holiday ...!)
• locally for glaucoma (timolol)
24
Q

Uptake of catecholamines: Uptake 1

A

Neuronal; due to the secondary active transporter NAT (Noradrenaline transporter)

Main mechanism for terminating the actions of Nad

Cotransports Na+, Cl- and catecholamine

Inhibitedby: cocaine
tricyclic antidepressants (desipramine)
25
Q

Inhibitors of noradrenaline uptake

A

NAT inhibitors enhance the effects of sympathetic activity
NAT is closely related to the dopamine and serotonin transporters (DAT and SERT)
Desipramine - tricyclic antidepressant
- major action is on CNS
- adverse effects: tachycardia, dysrhythmia
Cocaine - euphoria and excitement (CNS action)
- tachycardia and increased BP (peripheral)
- also a local anaesthetic

26
Q

Mono-amine oxidase inhibitors

A

Most block MAO irreversibly
Used clinically as antidepressants
Increase levels of noradrenaline, dopamine and 5-HT in the brain and peripheral tissues (similar to nervous system innervation)
Adverse effects include postural hypotension, weight gain, restlessness, insomnia, cheese reaction (hypertensive episode following ingestion of tyramine- containing food, e.g. cheese; flushing)
Examples
- phenelzine, tranylcypromine, iproniazid
- moclobemide (reversible, competitive inhibitor)

27
Q

Indirectly acting sympathetic amines

A
  • e.g. Amphetamine, ephedrine, tyramine,
  • Structurally related to noradrenaline
  • Transported into nerve terminals (NAT) and into vesicles (VMAT)
  • Displace noradrenaline, which leaks out via NAT
  • Similar effect on dopamine and 5-HT in CNS
  • Long-lasting effects that mimic those of noradrenaline: bronchodilatation, vasoconstriction, +ve inotropy, raised BP
  • CNS effects underlie their use as substances of abuse

NAS (33 decks)

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