Autonomic and NMJ Pharmacology Flashcards
How many types of cholinergic receptors exist?
2, ionotropic (ion channel nicotinic receptor) and metabotropic (g-protein)
How many types of adrenergic receptors exist?
1, metabotropic
What is the function of presynaptic autoreceptors?
Once bound to the transmitter, they will inhibit voltage gated Calcium channels and reduce further transmitter release
Where is the neurotransmitter usually metabolised?
Within the cell
What are the two components of the NMJ?
Efferent motor neurones and the skeletal muscle
Give examples of how you could stop the NMJ synapses working well?
Stop acetylcholine being packaged into vesicles
Stop vesicle release by blocking calcium channels
Stop vesicle release by preventing vesicle fusion
Blocking post synaptic nicotinic receptors
Use an agonist to keep these receptors open, causes brief muscle twitching and then paralysis as voltage gated channels stay in their refractory state
How can you make the NMJ synapses work better?
Prolong action potential, by letting in more calcium ions and releasing more acetylcholine
Stop the breakdown of acetylcholine by blocking the enzyme acetylcholinesterase
What can depolarizing and non-depolarizing blockers be used for paralysis?
Surgical procedures, controlling spasms in tetanus
What can anticholinesterases be used for?
Treating myasthenic conditions
Reversing action of non-depolarizing blockers
Stops the breakdown of Ach by blocking the acetylcholinesterase so it hangs around in the synaptic cleft for longer.
How can you stop transmission in the ANS at the ganglion?
The receptors are the same, so same methods apply
Why can you activate nicotinic receptors at the ganglion using Nicotine but not at the NMJ?
Nicotine is more potent at the ganglion
Why are there no clinical applications of ganglionic transmission modulation?
Drugs modulate parasympathetic and parasympathetic ganglionic transmission and probably NMJ transmission too, producing complex actions with many side-effects
What is the effect of muscarinic agonists?
Mimics the effect of the parasympathetic nervous system
What is the effect of a muscarinic antagonist?
Blocks the effect of the parasympathetic system
What is gluacoma characterised by?
High intraoccular pressure
Where does aqeous humour normally drain?
Through the trabecular network into the canal of schlemm
How can drainage of aqueous humour be increased?
Muscarinic agonists - contract ciliary muscle - opening up the trabecular network
Makes the sphincter muscle of the eye contract which has the same effect.
How can you inhibit post ganglionic sympathetic transmission?
Block enzymes that produce noradrenaline
Stop the Noradrenaline being packaged into vesicles
Introduce fake transmitter which doesn’t ave the same effect as NA
Inhibit release by activating presynaptic autoreceotors (inhibiting voltage gated calcium channels and therefore inhibiting calcium dependant exocytosis)
What are sympathomimetics and give examples?
Things that make the sympathetic post ganglionic synapses work better
Some sypathomematics indirectly trigger the release of NA - amphetamine
Some sympathomematics are agonists of NA which activate specific alpha and beta receptors
Things that stop the breakdown of NA have little effect because they are inactivated by uptake, and the breakdown only occurs inside cells.
What is a clinical application of a alpha 1 agonist?
Stops watery secretions in the mouth and airways, used as decongestants and to dilate the pupil
What is a clinical application of a alpha 2 agonist?
Treatment of hypertension- reduces heart rate and strength of contraction
What is a clinical application of a beta 2 agonist?
Treatment of asthma, relaxes the muscles in the airways of the lungs
What is a clinical application of a beta 1 antagonist?
Treatment of hypertension, angina, arrhythmias and gluacoma, reduces the production of aqueous humour.
What is noteworthy about parasympathetic muscarinic antagonists?
Not selective and will block all three types of muscarinic receptor – M1, M2 and M3
