Session 8.3: The ANS: Pharmacological Intervention in ANS - Cholinergic Transmission Flashcards
where do interventions occur
point of chemical communication
what are the most basic steps in neurotransmission
- uptake of precursors
- synthesis of transmitter
- vesicle storage of transmitter
- degradation of transmitter
- depolarisation of propagated action potential
- depolarisation-dependent influx of calcium ions
- exocytotic release of transmitter
- diffusion to post synaptic membrane
- interaction with post synaptic receptors
- inactivation of transmitter by enzymatic activity
or - re uptake of transmitter to move out of synpatic cleft
- interaction with pre synaptic receptors
neurotransmitter can either be repackaged or degraded
what steps are pharmacologically manipulated
4, 9, 10, 11, 12
where does cholinergic transmission occur
cholinergic - all transmission at ganglia and all transmission at parasympathetic nervous junction
how is acetylcholine synthesised
acetyl coA + choline -> acetylcholine + enzyme A
by choline acetyltransferase
how is acetylcholine degraded
terminals are coated with the enzyme acetylcholinesterase (outer surface of membranes)
acetylcholine -> acetate + choline
how does cholinergic transmission occur
acetylcholine synthesised and packaged and released on appropriate demand. can bind with nicotinic ACh at post junctional membrane or can be mtabolised by anticholinesterases
if ganglion synapse
nicotinic ACh receptor
how have we intervened in cholinergic transmission in hypertension
drugs have actions selectively at autonomic ganglia - blocking drug, trimethaphan - control hypertension during surgery and used in hypertensive emergencies
why are neuromuscular junctions unaffected by drug blocks autonomic ganglia
differ in structure
how have we intervened in cholinergic transmission in hypertension in alzeihmers or myasthenia gravis
acetylcholinesterase inhibitors - increase activity of released ACh = eg: pyridostigmine to treat myasthenia gravia and donepezil to treat alzheimers
what other receptors can be targeted
muscarinic acetylcholine receptor - but difficult
how can cholinergic drugs cause side effects
they are not very selective
so if a non selective muscarinic ACh receptor agonist = autonomic side effects, decrease in HR, bronchoconstriction, increase sweating
what is sludge syndrome
observed changed in a patient with increase in parasympathetic nervous system. due to prolonged over stimulation of muscarinic acetylcholine receptors innervated by parasympathetic NS
what does SLUDGE stand for
Salvation: stimulation of salivary galnds
Lacrimation: stimulation of lacrimal glands
Urination: relaxation of utheral internal sphincter muscle and destrusor muscle contraction
Defecation
Gastrointestinal upset: smooth muscle tone change causing GI problems such as diarrhoea
Emesis: vomitting
