Autonomic nervous system Flashcards
amino acid transmitters
GABA, glutamate, glycine
monoamines
- catecholamines : noradrenaline, adrenaline, dopamines
- indoleamines : seratonin
- histamine
quatenary amines
aka choline esters
e.g. acetylcholines
function of ANS
ANS = autonomic nervous system
- homeostasis
–> parasympathetic drive = rest/repose
–> sympathetic drive = fight/flight (also during exercise)
= not all viscera and vasculature innvervated by both systems - contraction/relaxation of smooth muscle
- all exocrine/some endocrine secretions
- heart rate + contractions
- metabolism
anatomy of ANS (PNS)
CNS : brain & spinal cord
PNS : somatic (voluntary), autonomic (involuntary), enteric (gut health; involuntary)
Autonomic = parasympathetic and sympathetic –> same organs
parasympathetic
craniocaudal/craniosacral :
cranial = cranial nerves
caudal = sacral spinal nerves e.g. lower GI tract, bladder, genitalia
sympathetic
thoracolumbar:
3 major outflows=
1) prevertebral ganglia
2) paravertebral ganglia
3) adrenal medulla
organisation of ANS
CNS —-1st——-> ganglion —–2nd—–> effector organ
1st = preganglionic fibre
2nd = postganglionic fibre
para : long 1st and short 2nd
sym : short 1st and long 2nd
viscera and vasculature
viscera : internal organs of the body, especifically in the chest (heart, lungs) or abdomen (liver, pancreas or intestines).
vasculature : the blood vessels or arrangement of blood vessels in an organ or part.
SAM
sympathetic adreno medullary system
the sympathetic adrenomedullary system = the interaction between the sympathetic nervous system and the adrenal medulla.
the sympathetic nervous system is activated –> it sends signals to the adrenal medulla –>responds by releasing hormones directly into the bloodstream.
The main hormones released are epinephrine (adrenaline) and norepinephrine.
neurotransmitters (slide 12 of lecture 4)
Somatic motor/efferent system
–> releases acetylcholine at skeletal muscle/neuromuscular junctions
- acts on nicotinic acetylcholine receptors
Parasympathetic nervous system
preganglionic neurone + postganglionic neurone are cholinergic
preganglionic neurone = nictoninc acetylcholine receptors
postganglionic neurone = muscarinic acetyl choline receptors on effectors
Sympathetic nervous system
preganglionic neurone = always cholinergic (releases acetylcholine)
–> binds to nicotinic acetylcholine receptors on adrenal medulla
postganglionic neurone = always adrenergic = release noradrenaline
–> receptors on effectors e.g. smooth muscle, salivary glands and cardiac muscle
+ muscarinic acetylcholine receptors releases Acetylcholine onto sweat glands
acetylcholine synapse
- acetyl CoA +choline = acetylcholine
- stored in vesicles and released into the synapse
- broken down by AChE as acetate and choline (acetylcholinesterase)
- choline is used to make ACh again
ACh receptors
1) mAChR (muscarinic receptors)
–> muscarine is selective agonist = binds and activates muscarine receptors
–> G protein coupled receptors
2) nAChR (nicotinic acetylcholine receptors)
–> nicotine is selective agonist
–> ligand gated ion channels
drugs to active mAChRs in the PSNS
1) pilocarpine = makes pupils smaller –> treat glaucoma
2) bethanechol = contract detrusor muscule and relax sphinctor –> treat urinary retention
3) lacrimal/salivary glands secretion
4) cardiac muscle relaxation
5) gastric acid secretion
6) GIT muscle contraction = increased motility
drusg that block mAChRs in PSMS (antagonists)
1) tropicamide = inhibit pupillae constrictor muscle for dilation of pupil –> mydriasis
2) oxybutynin = inhibit detrusor muscle contraction and prevent sphinctor muscle relaxation –> urinary incontinence
3) ipratropium = inhibit bronchial smooth muscle contraction –> COPD
4) pirenzepine = blocks signal so less gastric acid is released –> peptide uclers
5) hyoscine = relax cobtraction of GI muscles and reduce spasms + discomfort –> IBS
noradrenaline synapse
- dopamine is precursor to noradrenaline
- dopamine beta hydroxylase converts dopamine –> noradrenaline
- Noradrenaline is stored in these vesicles until it is ejected into the synaptic cleft, typically after an action potential causes the vesicles to release their contents
Once in the synapse, noradrenaline binds to and activates receptors
After an action potential, NA molecules become unbound from their receptors. They are then absorbed back into the presynaptic cell by the noradrenaline transporter (NAT).
Once back in the cytosol, noradrenaline can either be broken down by monoamine oxidase or repackaged into vesicles by VMAT, making it available for future release.
- packaged into vesicles and released into synapse
- noradrenaline returns to cell through noradrenaline transporter (NAT)
Adrenergic
all are G protein coupled receptors
* alpha-adrenoceptors : 2 types = a1 and a2
* Beta-adrenoceptors : 3 types = B1, B2, B3
adrenaline = released from adrenal medulla
–> much higher affinity for B2> B1/B3/a
noradrenaline = released from nerves
–> much higher affinity for a> B1 and a lot less B2
these adrenoceptors are all excitatory (some alpha ones are inhibitory)
ACTIVATED adrenergic receptors in
the SNS?
mydriasis = noradrenaline binds to α1-adrenoceptors on radial muscle contraction –> pupil
- Detrusor muscle relaxation/sphincter muscle contraction
- Cardiac muscle contraction
- salbutamol (drug) agonises β2 adrenoceptors to relax bronchial smooth muscle
- phenylephrine used in nasal congestion, agonises α1 adrenoceptors to restrict blood flow and mucosal secretion by vasoconstriction
- GIT muscle relaxation => decreased motility
- What would happen if I BLOCKED adrenergic receptors in the SNS?
Timolol = competes with norepinephrine = blocking β1 receptors = inhibits the effects of sympathetic stimulation on the heart = prevent heart rate and force of contraction in hypertension
- Inhibit radial muscle => miosis
- Inhibit detrusor muscle relaxation and prevent sphincter contraction
- Inhibit bronchial smooth muscle relaxation
- Vascular smooth muscle relaxation e.g. prazosin blocks α1 adrenoceptors so noradrenaline can’t bind to dilate vasicalar smooth muscle// blocks vasoconstriction leading to vasodilation and reduce arterial blood pressure
- Inhibit GIT muscle relaxation => increase motility
Muscarinic ACh Receptors
M1 (“neural”)
M2 (“cardiac”)
M3 (“glandular/
smooth muscle”)
M1 (“neural”)
location:
* CNS
* Autonomic ganglia
* Glands: gastric, salivary = Secretion
* git : Contraction (increased motility); gland secretion; relaxation of sphincters; gastric acid secretion
–> excitatory
M2 (“cardiac”)
Location:
1) Heart: SA note, AV node, atria, ventricles
Decreased rate of contraction (SA node); decreased automaticity (AV node) -> rate at which the AV node generates electrical impulses independently decrease so fewer impulses produced; decreased force of contraction (atrial muscle)
2) CNS
–> Inhibitory
M3 (“glandular/
smooth muscle”)
Location
1) Smooth muscle: GIT, eye, airways, bladder
2) Glands: gastric, salivary Secretion
3) Blood vessel endothelium
eye : Contraction and accommodation of lens/ Contraction of pupillae sphincter muscle and miosis
airways : Contraction of smooth muscle (constriction); gland secretion
GIT : Contraction (increased motility); gland secretion; relaxation of sphincters; gastric acid secretion
bladder : Contraction of detrusor muscle; relaxation of sphincter
–> Excitatory
