7. Cholinoreceptor antagonists Flashcards
what is affinity?
the ability of a drug to bind to a particular receptor to form a complex
reversible reaction
both antagonists and agonists have affinity
what is efficacy?
the ability of a drug to stimulate a response after binding to the receptor
only agonists have efficacy
what are nicotinic receptor antagonists also called and what do they do?
ganglion-blocking drugs
they interfere with transmission through all ganglia (sympathetic and parasympathetic)
what are the 2 actions of nicotinic receptor antagonists?
- block the nicotinic receptor (ion-channel linked receptor) to prevent depolarisation as the ion channel cannot open
- block the channel (drug sits in the channel pore and prevents ion passage)
give 2 examples of nicotinic receptor antagonists
hexamethonium
trimetaphan
describe the uses and effects of hexamethonium
- first anti-hypertensive drug
- causes vasodilation because the antagonist blocks the sympathetic tone in vessels
- causes decreased renin secretion because less aldosterone is released
describe the uses and effects of trimetaphan
- used clinically
- i.v. during surgery to induce hypotension
- short-acting drug to reduce the chance of blood loss during surgery
describe use-dependent block
the more open the channel is, the more effective the block
more agonist -> ion channels open more -> antagonist blocks channels more
how can you overcome a block of the actual nicotinic receptor?
by adding more acetylcholine (competitive)
do ion channel blockers have affinity?
no
what widespread effects do hexamethonium and trimetaphan have on the body?
- pupil constriction interference -> dilation
- bladder dysfunction due to bladder smooth muscle impairment
- decreased GI tone
- decreased saliva production
- impaired sweating capacity
- decreased exocrine secretions
why are ganglion blocking drugs good anti-hypertensive drugs?
by blocking renin secretion and stopping vasoconstriction (sympathetic) rather than reducing heart rate and contractility (parasympathetic)
do hexamethonium and trimetaphan block the receptor or the channel pore?
hexamethonium - both
trimetaphan - receptor
what is alpha-bungarotoxin and how is it different to nicotinic antagonist drugs?
it is a poison that comes from the common krait snake (potent toxin)
DIFFERENCE:
- it binds irreversibly (with covalent forces)
- it targets both the autonomic and somatic nervous system causing paralysis
what do muscarinic receptor antagonists influence?
parasympathetic function (except sweat glands which sympathetic nerves innervate via muscarinic receptors)
give 2 examples of muscarinic receptor antagonists
atropine
hyoscine
(structurally similar to ACh)
what are the effects of atropine on the CNS?
normal dose: little effect
toxic dose: mild restlessness, agitation (CNS excitation)
what are the effects of hyoscine on the CNS?
normal dose: sedative, amnesia
toxic dose: CNS depression, paradoxical CNS excitation (associated with pain)
what is tropicamide?
the ophthalmic drug (muscarinic receptor antagonist) that blocks muscarinic receptors in the iris and causes pupil dilation
why is tropicamide useful?
it allows you to examine the retina at the back of the eye using a light
why might muscarinic receptor antagonists be used before a surgical procedure as anaesthetic premedication?
- reverses constriction in lungs -> bronchodilation -> assists inhalation of anaesthetic
- dries up salivary secretions -> reduces risk of aspiration of fluid back down into the lungs
- counteracts the way the anaesthetic slows down HR by increasing it
- hyoscine is a sedative -> calms patient
what is motion sickness due to?
a sensory mismatch - the sensory info coming in visually does not match the sensory info coming in through the labyrinth (regarding balance and posture) so when it doesn’t match up the vomiting centre may be activated
how can hyoscine patches help motion sickness?
hyoscine gets into the brain and prevents the cholinergic system from activating the vomiting centre
how do dopaminergic neurones control movement?
dopaminergic neurones originate from substantia nigra -> project down to striatum -> dopamine is released in striatum and binds to D1 receptors on striatal neurones -> control of movement
