Cholinoreceptor antagonists Flashcards
Explain affinity and efficacy relating to both agonists and antagonists.
Only agonists posses efficacy
Antagonists + agonists possess affinity.
Affinity = how strongly + specifically a drug binds.
Efficacy = the significance of the effect generated by binding.
Where are nicotinic ACh receptors located in the nervous system?
All pre-ganglionic synapses
Give another name for nicotinic receptor antagonists.
Ganglion blocking drugs.
What 2 types of drugs are considered nicotinic receptor antagonists?
Receptor antagonists and ion channel blockers.
Name a nicotinic receptor antagonist that blocks the receptor and one that blocks an ion channel.
Ion channel - hexamethionium
Receptor - trimetaphan.
What is meant by use dependent block with reference to ion channel blockers?
The more the channel is in use, the more effective the block of the channel by the drug.
Do ion channel blocker drugs have affinity?
No, since they only blockthe receptor, not bind to it.
Since nicotinic receptor antagonists effect both the PNS and SNS, what are the effects of administering them?
It depends upon which system is more active at that specific time - at rest, PNS is dominant, so the effect of the PNS at the point would be lost.
e.g. at rest, heart rate increases since PNS largely controlls heart rate at rest and keeps it low.
Outline the ffects of nicotinic receptor antagonists at rest.
Heart rate increases.
Pupil relaxation.
Bronchodilation.
Detrusor dilation.
Reduced gut motility.
Why does hexmathonium act as an anti-hypertensive, even though it increases heart rate by reducing PNS innervation to the heart?
PNS innervation of VSMC –> dilation which reduces TPR.
Reduced renin secretion from kidney –> reduced salt reuptake so reduced water retention –> reduced blood volume and reduced TPR. AGT II is also a powerful hypertensive, and is produced less.
What exocrine effect does reduced PNS innervation have?
Increased secretions, e.g. sweat, gut secretions, saliva.
Wnat is the primary use of Trimetaphan?
Short acting anti-hypertensive during surgery.
How does alpha-bungarotoxin antagonise the nicotinic receptor?
Covalently binds to receptor - it must be replaced to restor function.
Why is alpha-bungarotoxin dangerous?
Paralysis of skeletal muscle.
What is the problem with using nicotinic receptor antagonists therapeutically?
They effect the entire nervous system - side effects are too broad.
Where are muscarinic receptors located?
