Pharmacology 1 - Intro to the ANS Flashcards
List the targets and functions of the ANS
- Eye (dilation/costriction of pupil + contraction of ciliary muscle)
- Trachea/bronchioles
- Glycogenolysis/ gluconeogenesis in the liver
- Lipolysis in adipose
- Increased renin secretion in the kidney
- Ureters and bladder (detrusor, trigone and sphincter)
- Salivary glands
- Skin (piloerection/ sweating)
- Heart
- GI motility and spincters
- Blood vessel dilation/constriction
What neurotransmitters are used in the ANS?
- PNS uses ACh always
- Sympathetic - pregnaglionic releases ACh, postganglionic nerve releases NA at effector organ/ released from adrenal medulla, only using ACh at sweat gland
What neurotransmitter is used by the somatic NS?
ACh
What receptors does acetylcholine bind to?
- Membrane bound receptors
- Either muscarinic or nicotinic
Where are nicotinic receptors used?
- PNS ganglia
- SNS ganglia
Where are muscarinic receptors used?
- At effector organs
Describe the features of nicotinic receptors
- Nicotinic used at autonomic ganglia
- Stimulated by nicotine/acetylcholine
- Type 1 - ionotrophic (ion channel linked) - important as it needs to be fast.
- If manipulated will affect the whole ANS
Describe the features of muscarinic receptors
- At all effector organs innervated by PNS and also by SNS where acetylcholine is used
- Stimulated by muscarine/ acetylcholine (agonist)
- Type 2 - G-protein coupled receptor - slower process
List the sub-types of muscarinic cholinoceptors and their uses
- M1 - CNS, salivary gland, stomach (forebrain - learning/memory)
- M2 - Cardiac (brain - inhibitory autoreceptors)
- M3 - Exocrine, salivary glands, sweat glands and eye & smooth muscle (hypothalamus - food intake)
[- M4 - Periphery (CNS prejunctional nerve endings - inhibitory) - M5 - CNS striatal dopamine release]
List the qualities of adrenoceptors
- At all effector organs innervated by postganglionic sympathetic fibres
- Stimulated by noradrenaline/adrenaline
- Type 2- G-protein coupled
Describe the process of ACh production and release
- Acetyl coA + choline makes ACh + coA (via choline acetyl transferase)
- ACh released from vesicles following action potential and calcium influx
Describe the process of ACh metabolism
- Converted to choline + acetate via acetylcholinesterase
- Breakdown products are then reused to make more acetylcholine
Describe the stages involved in noradrenaline production and release
- Tyrosine to DOPA via tyrosine hydroxylase
- DOPA to dopamine via DOPA decarboxylase
- Dopamine to noradrenaline via dopamine B in the vesicle
- Released from vesicles following action potential and calcium influx
Describe the process of Noradrenaline metabolism
- Removed by transport proteins into the membrane - no enzyme in the synapse so NA stays in the synapse for a longer time
- Metabolised in the presynaptic neuron to metabolites in the mitochondria, via Monoamine oxidase A
- Degraded via COMT in the prostsynaptic neuron
What is responsible for the cephalic and gastric phase of digestion?
PNS
Does PNS or SNS have the most effect on intrinsic heart rate?
PNS
Compare PNS and SNS divergence
- PNS is localised and discrete, 1:1 ratio of pre:post ganglionic neurones
- SNS is coordinated and very divergent, with up to 1:20 ratio of pre:postganglionic neurones
What controls the enteric nervous system?
- PNS and SNS
- Also local control via the environment of the gut
What effect would blockade of nicotinic acetylcholine receptors have on heartrate
- At rest
- During exercise?
- At rest heart rate would increase as PNS is inhibited
- During exercise less of a rise as SNS is in control - no nicotinic receptors involved
List the subtypes of adrenoreceptors
- a1
- a2
- B1
- B3
Where is the drug target for acetylcholine the stomach?
- Muscarinic receptors at the stomach
- In the smooth muscle/ acid releasing cells/ endocrine cells that release histamine
- Increase contraction/ acid production/ histamine production
Where is the drug target for noradrenaline when controlling heart rate?
- B1 adrenoceptor in the nodal tissue
- Would increase heart rate
How is adrenaline produced?
- From noradrenaline via PNMT
- In chromaffin cells in the adrenal medulla
How is adrenaline metabolised?
Degraded by COMT to metanephrine then to VMA (vanillylmandelic acid via monoamine oxidase)
What is mydriasis?
Pupil dilation
What is miosis?
Pupil constriction
