ANS Flashcards
what does the ANS do?
controls involuntary functions
e.g heart rate, blood pressure, GI motility , iris diameter
what are the two divisions of the ANS and what do they do
sympathetic- responds to stressful situation. fight or flight response. increases heart rate, force of contraction and blood pressure.
parasympathetic-regulates basal activities. rest and digest.
which regions of the spinal column do the two divisions arise from
parasympathetic-cranial and sacral region
sympathetic- thoracic and lumbar
describe the general structure of the ANS
pre-ganglionic and post ganglionic parts
ganglion is part at which synapses occur
pre-ganglionic part is myelinated
what neurotransmitters r used in the ANS
ACh and noradrenaline
all pre ganglionic neurone are cholinergic (use ACh) and activate nicotinic ACh receptors (ligand-gated ion channels)
parasympathetic post-ganglionic neurons are also cholinergic (release ACh that acts on muscarinic ACh receptors, these are GPCRs )
most sympathetic post-ganglionic neurons are noradrenergic
what does NA interact with
adrenoceptors
two classes- alpha and beta
can be further divided into a1,a2,b1,b2
what type of receptors are m1-m5 muscarinic acetylcholine receptors and all adrenoceptors
GPCR
not all sympathetic post-ganglionic neurons are noradrenergic. what re the exceptions?
they are instead cholinergic
-those innervating sweat glands, hair follicles
release ACh that acts at muscarinic ACh receptors
sympathetic postganglionic neurons in the adrenal glands
differentiated to from neurosecretory chromaffin cells
chromatin cells can be considered as postgamglionic sympathetic neurons that do not project to a target tissue, instead release adrenaline into blood stream
what does parasympathetic release of ACh cause in the heart and what receptor type
SA node- bradycardia
AV` node- reduced cardiac conduction velocity
M2
what does parasympathetic release of ACh cause in smooth muscle and what receptor type
M3 bronchial contraction increased intestinal mobility/secretion bladder contraction and relaxation penile erection ciliary muscle and iris sphincter contraction
what does parasympathetic release of ACh cause in glands and what receptor type
M1/M3
increased sweat/ salivary /lacrimal secretion
what does sympathetic release of NA cause in the heart and what receptor type
SA node- tachycardia
ventricles- positive inotropy
B1
what does sympathetic release of NA cause in smooth muscle and what receptor type
arterial contraction(a1) in non flight essential arterioles and relaxation in essential ones (b2) bronchiolar relaxation -b2
how is the output from the ANS regulated
afferent/sensory inputs
e.g blood o2 detected by carotid body , chemoreceptors etc
sensory neurones monitor co2, o2 and nutrients in blood
most common sites of drug action in neurotransmission
degradation of neurotransmitter
interaction with post synaptic receptors
inactivation of transmitter
re-uptake
interaction with pre ganglionic receptors
acetylcholine synthesis equation
acetyl CoA +choline (from diet)——–> acetylcholine +coenzyme A
enzyme is choline acetyltransferase
ACh is packed into vesicles here
ACh degradation equation
ACh———->acetate +choline
this is when ACh is released from vesicle
enzyme is cholinesterase
why can drugs have actions selectively at autonomic system
give example
nicotinic acetylcholine receptors at autonomic ganglia and the neuromuscular junction differ in structure therefore can have actions selectively
e.g ganglion blocking drug trimethaphan (antihypertensative)
what is the problem with cholinergic cells and what would a non-selective muscarinic EACh receptor agonist do
lack of sensitivity unwanted side effects decrease heart rate and cardiac output increase bronchoconstriction increase sweating and salivation
what is SLUDGE syndrome
pathological effects of massive discharge of parasympathetic NS
Salivation: stimulation of the salivary glands
Lacrimation: stimulation of the lacrimal glands
Urination: relaxation of the internal sphincter muscle of urethra, and contraction of the detrusor muscles
Defecation
Gastrointestinal distress: Smooth muscle tone changes causing gastrointestinal problems, including cramping
Emesis: Vomiting[
when is sludge syndrome encountered
drug overdose
ingestion of magic mushrooms
exposure to organophosphorus insecticides
exposure to nerve agents
the last two agents covalently modify acetcholinesterase to irreversibly deactivate enzyme and rats ACh levels
what are the symptoms of SLUDGE due to
prolonged stimulation of muscarinic ACh receptors in rogans and muscles innervated by PNS.
how is sludge treated
atropine
pralidoxime
