Autonomic nervous system Flashcards
What does β2 adrenocepter activation result in?
- Increased heart rate and force of contraction
- Blood vessels to muscles dilate, for inc oxygen
What does α adrenoceptor activation result in?
- Constriction of blood vessels to the gut and skin
- Dilation of blood vessels to pupils to enhance vision
- Negative feedback inhibition of transmitter release
What are the similarites and differences between PNS and SNS signalling anatomy?
PNS: long preganglionic neurons, muscarinic ACh receptors on effectors
SNS: short preganglionic neurons, adrenoreceptors on effectors
Both use nicotinic ACh receptors (ganglia) bc they both use ACh as a neurotransmitter
What are the two exceptions to the SNS typical signalling pathway?
- Adrenal medulla: pre-ganglionic neuron goes straight to adrenal medulla, where chromaffin cells release adrenaline and NAd into blood
- Sweat glands: post-ganglionic neuron releases ACh, received by muscarinic AChR on sweat gland
Which system does muscarine impact and how?
Parasympathetic nervous system
Non-selective agonist of muscarinic receptors (similar strucutre to ACh) – its poisonous
Which cholinomimetic drugs indirectly activate mAChRs?
muscarinic ACh receptors
- Reversible inhibitors of ACh-esterase: physostigmine – tertiary plant alkaloid.
- Irreversible inhibitors of ACh-esterase: organophosphates eg sarin gas poisoning.
What are the effects of activating muscarinic receptors?
Heart: decrease force/rate
Pupils: contract
Bronchi: contract
GI tract: contract
Veins/arterioles: dilate
even though not usually seen in PNS
How can cholinomimetic drugs treat glaucoma?
Contraction of the pupil constrictor (miosis) and ciliary muscle by muscarinic receptor activation widens the anterior angle of the eye and promotes drainage of aqueous humour through the Canal of Schlemm
Eg Ecothiophate, Pilocarpine
The underlying cause of glaucoma is a problem with secretion or drainage of aqueous humour. The resulting increase in intra-ocular pressure is painful, and can damage the optic nerve and retina.
How can cholinomimetics treat Intestinal atony and Urinary bladder atony?
Increase peristalsis by activating M3 on bladder detrusor muscle
Eg. Bethaneco, Neostigmine
What are the effects of anti-muscarinics? Give an example
They are antagonists and block muscarinic receptor function, basically opposite of what cholinomimetics do
eg Atropine (from nightshade)
What are some theraputic uses of anti-muscarinics?
- Pre-anaesthetic medication: reduces saliva and lung mucus
- Ophthalmological uses: dilates pupil
- Gastrointestinal antispasmodic agents: relaxes GI smooth muscle
- Treatment of poisoning by cholinomimetics
How is noradrenoline synthesised and stored?
Secreted and stored in the sympathetic presynaptic nerve terminal
- L-tyrosine-> L-DOPA (by tyrosine hydroxylase) -> dopamine (by DOPA decarboxylase) -> NA (by dopamine b-hydroxylase) -> vesicles
A transporter protein in the vesicle membrane
driven by an H+ gradient concentrates NA in the vesicle (0.3 to 1.0mmol/L)
What affect do activated α2-adrenoceptor have on NA release?
Negative feedback, NA stimulates these receptors and they inhibit further release of NA
α2-adrenoceptors inhibit the enzyme adenylyl cyclase which normally produces cAMP. This reduction in
cAMP was suggested to lead to inhibition of presynaptic Ca2+ channels and thus reduce Ca2+ entry into the
terminal. More recent evidence suggests that direct action of a G-protein on the Ca2+ channel mediates this
effect of α2 receptors
What are the 2 mechanisms of NA uptake?
- NA goes back to synaptic terminal, high affinity but low max rate, co transports Na and Cl with NA. MAO metabolises it
- NA goes into non-neuronal glilal cells, low affinity but high max rate. COMT metabolises it
monoamine oxidase (MAO)
catechol-O-methyl transferase (COMT)
What do α2 adrenorecptors do?
Inhibit adenylyl cyclase, so reducing cAMP production
