Pharmacology of ANS

Question 1

Pharmacological manipulation of ganglionic transmission?

Answer 1

You could target transmission at the autonomic ganglia with any of the drugs that affect the NMJ
However, it will affect both sympathetic and parasympathetic ganglia leading to complex effects with many side effects
There are no clinical applications

Question 2

What was the first evidence that we have diff types of nicotinic receptors?

Answer 2

The only (quite) interesting point is that hexamethonium blocks nicotinic receptors at the autonomic ganglia but not the NMJ

Question 3

What are the 2 ways to modulate parasympathetic post ganglionic transmission?

Answer 3

Muscarinic receptor agonists (e.g. carbachol, pilocarpine)

Muscarinic receptor antagonists (e.g. atropine)

Question 4

Describe
Muscarinic receptor antagonists (e.g. atropine)?

Answer 4

Block effects of the parasympathetic system

Question 4

Describe Muscarinic receptor agonists (e.g. carbachol, pilocarpine)
?

Answer 4

Mimic the effect of the parasympathetic system

Question 5

How are muscarinic agonists used in treatment of glaucoma (high intraocular pressure)?

Answer 5

Aqueous humour normally drains through the trabecular network into the canal of Schlemm
Muscarinic agonists contract the ciliary muscle supporting the lens and contracts the sphincter muscle of the pupil
Depending who you read, one or both of these opens up the trabecular network and increase drainage of the aqueous humour

Question 6

What is glaucoma?

Answer 6

the vitreous humour in eye (liquid) is not able to drain properly which causes high intraoccular pressure that can lead to death of retinal ganglion cells and can damage optic nerve

Question 7

How can we modulate sympathetic post ganglionic transmission?

Answer 7

inhibiting transmission:
Block the enzymes that produce noradrenaline (e.g. carbidopa)

Introduce a “false” transmitter (e.g. methyldopa)- similar to noradrenaline and will get recognized by transporter, brought into cell , metabolized into methylnoradrenaline and released into synaptic cleft. Cannot bind to receptors and production of noradrenaline decreased

Activate inhibitory presynaptic (α2) autoreceptors (e.g. methyldopa)

Block α or β postsynaptic receptors (e.g. doxazosin or propranolol)

Potentiating transmission:

Stimulate noradrenaline release (e.g. amphetamine)
Inhibit uptake into neurons (e.g. cocaine and tricyclic antidepressants) or glia (e.g. phenoxybenzamine)
Activate postsynaptic receptors (e.g. phenylephrine and salbutamol)

Question 8

Clinical applications of adrenergic receptors agonists and antagonists ?

Answer 8

α1 agonists as decongestants and to dilate the pupil (mydriatics)

α2 agonists for the treatment of hypertension

β2 agonists for the treatment of asthma

β1 antagonists for the treatment of hypertension, angina and cardiac arrhythmias