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Flashcards in Introduction to the ANS Deck (48):

What is meant by pharmacodynamics

What drugs do to the body- their effects


What is meant by pharmacokinetics

How the body responds to the drugs (metabolism, excretion)


Describe the basic function of the ANS

Peripheral functions- not conscious


What are the 3 outputs (branches) of the CNS

§ There are 3 branches to the CNS; the ANS, the somatic nervous system and the neuroendocrine syste


What does the ANS act on

exocrine glands
smooth muscle
cardiac muscle
host defence


What does the somatic nervous system act on

skeletal muscle,
including the diaphragm and respiratory muscle


What does the neuroendocrine system act on

growth, metabolism, reproduction, development,
salt & water balance,
host defence


List some examples of the ANS in action

§ Some targets of the ANS include:
o Pupillary constriction – constriction mediated by the PNS via the oculomotor nerve (CNIII).
o Cephalic and gastric phases of digestion – vagal nerve PNS mediation.
o Basal heart rate – PNS is dominant at rest (as the intrinsic rate is 100-110bpm which isn’t normal at rest) however as baroreceptors stretch less as BP drops, less inhibition of SNS leading to increased heart rate.


Describe the effect of reduced baroreceptor firing

Loss of fluid (e.g excessive sweating)- BP decreases- decreased rate of firing of arterial baroreceptors- therefore less inhibition of sympathetic neurones- the sympathetic neurone (split into two branches) can then act to increase heart rate, increase BP (vasodilation) and increased force of contraction of the heart


Do all targets have PNS and SNS innervation

Note that most targets in the body receive BOTH PNS and SNS innervation BUT some targets only receive one type branch of the ANS – examples include the blood vessels (only the SNS innervates).
2 opposing effects in blood vessels - NA constricts, histamine dilates
Lungs only receive PNS- dilation is by adrenaline in fight or flight response


Effects of ANS on the eye

Dilatation (Pupil) - symp
Constriction (Pupil)- para
Contraction (Ciliary Muscle)- para


Effects of ANS on trachea and bronchioles

Dilates (Ad)
Constriction- para


Effects of ANS on liver


Both symp


Effects of ANS on adipose

Lipolysis- symp


Effects of ANS on kidney

Increased renin secretion- symp


Effects of ANS on bladder and ureters

Relaxes detrusor; constriction of trigone and sphincter (symp)

Contraction of detrusor; relaxation of trigone and sphincter (para)


Effects of ANS on salivary glands

Thick, viscious secretion- sympathetic
Copious, watery secretion - para


Effects of ANS on skin

Piloerection - symp
Increased sweating (C)- symp (cholinergic)


Effect of ANS on heart

Increased rate and contractility- symp
Decreased rate and contractility- para


Effect of ANS on G.I system

decreased motility and tone, sphincter contraction- symp

increased motility and tone, increased secretions- para


Effect of ANS on blood vessels

to skeletal muscle- dilatation- symp
to skin, mucous membranes and splanchnic area)- constrition- symp


Summarise the characteristics of the PNS

o Has LONG pre-ganglionic fibres and SHORT post.
o ALL transmitters are ACh.
o Is DISCRETE – 1:1 pre- vs. post-.


Summarise the characteristics of the SNS

o Has SHORT pre-ganglionic fibres and LONG post.
o Releases mainly A and NA.
o Is DIVERGENT (mass discharge) – 1:20 pre- vs. post


Describe the exemptions of the SNS

ADRENAL GLAND- beaves like post-ganglionic fibre- only peripheral tissue to function like an autonomic nerve- 80% A and 20% NA

Sweat gland- Post ganglionic fibre releases Ach


Explain the exemption of the sweat gland

PSNS is involved in secretions- sweat is a secretion- but sweat needs to be SNS- so Ach was retained in evolution- despite being a SNS response


Why is it important that many pre ganglionic sympathetic fibres can have an effect on many post ganglionic fibres

SNS is involved in stress response- 1 pre ganglionic : many post ganglionic- multiple effects required

increase sweat with increased HR, BP and blood flow, whilst decreasing gut secretions


Summarise the enteric nervous system

network of neurones responding to the gut environment- can communicate and determine response- local signals- no need for brain - but ANS can influence ENS


Describe the enteric sensory neurones in action

Sensory neurone connected to mucosal chemoreceptors and stretch receptors detect chemical substances in the gut lumen or tension in the gut wall caused by food.
Information relayed to submucosal and myenteric plexus via interneurons.


Describe the enteric motor neurones in action

Motor neurones release acetylcholine or substance P to contract smooth muscle or vasoactive intestinal peptide or nitric oxide to relax smooth muscle.


Summarise the somatic nervous system

§ Very simple – just long neurones with eventual ACh release.


What are the Ach receptors

membrane bound- muscarinic or nicotinic


Summarise nicotinic receptors

At all autonomic ganglia
Stimulated by nicotine/acetylcholine
c) Type 1 - Ionotropic


Why is it important that nicotinic receptors are type 1- ionotropic

Swift signal- impoartant fasted method
ganglia linking pre to post
ligand binds (Ach leading to Ca2+ or Na+ influx in post ganglionic fibre)


Summarise the muscarinic receptor

At all effector organs innervated by
post ganglionic parasympathetic fibres and cholinergic sympathetic (sweat glands)
b) Stimulated by muscarine/acetylcholine
c) Type 2 – G-protein coupled


Summarise GPCRs

7-TM receptor
associated G-protein activated- starting I.C machinery (second messenger)- activation of cell signalling


Which of the following effects would be observed after blockade
of nicotinic acetylcholine receptors in an individual at rest?

Constipation- due to blockage of PNS- can't act on effectors


What effect would blockade of nicotinic acetylcholine
receptors have on heart rate;

At rest
During exercise

At rest- PNS is dominant- so HR will increase if PNS is blocked

During exercise- SNS is dominant during exercise- less of an increase (nicotinc receptor at pre-ganglionic sympathetic neurone blocked)


List the su-types of muscarinic cholioceptors

M1 – Neural (Forebrain – learning & memory)

M2 – Cardiac (Brain – inhibitory autoreceptors)

M3 – Exocrine & smooth muscle (Hypothalamus – food intake)

M4 – Periphery: prejunctional nerve endings (inhibitory)

M5 – Striatal dopamine release


Summarise adrenoreceptors

§ Found at all effector organs innervated by post-ganglionic SNS fibres (not sweat glands).
§ Stimulated by noradrenaline/adrenaline.
§ Type 2 – G-protein coupled.


Describe the location of the different adrenoreceptors

alpha 1- smooth muscle in blood vessels and bronchi, dilator pupillae- contraction
alpha 2- smooth muscle in blood vessels, presynaptically on adrenergic synapses- reduced NT release
beta 1- heart muscle, presynaptically on adrenergic symapses- increased HR and force of contraction, increased NT release
beta 2- smooth muscle in blood vessels and bronchi- relaxation


What do we need to consider for all drugs

What is the drug target?
e.g M3 muscarinic receptors

2. Where is the drug target?
e.g gastric S.M, Paneth cells, endocrine cels

3. What is the end result
of the interaction?
contraction, increased acid production, increased gastrin secretions


What happens when the NT binds to its receptor

it activates it and then it unbinds


Why do we have mechanisms to remove the NT

Don't want permanent activation
Want effect to be short lived
rapid activation with quick deactivation


Describe the biosynthesis of Ach

Acetyl coA (from mitochondria) + choline --- Ach + CoA ( Choline acetyltransferase)

Ach is packaged into vesicles -- action potential leads to Ca2+ influx- binds to vesicles- transported to pre-synaptic membrane- Ach released


Describe the metabolism of Ach

Ach can bind to post-synaptic receptor or to acetylcholinesterase (lots of this enzyme- eventually they will all bind to it) Ach converted to choline and acetate
choline taken back up by the nerve terminal- to make more Ach


Describe the biosynthesis of NA

Tyrosine is the precursor (delivered to nerve terminal by blood)
converted to DOPA ( Tyrosine hydroxylase)
DOPA --- Dopamine ( DOPA decarboxylase)

Dopamine is packaged into a vesicles

Dopamine --- NA (Dopamine B hydroxylase)

Release as normal


Describe the metabolism of NA

No enzyme in the synapse of sympathetic neurones- longer lasting effect

Uptake 1 protein- takes NA back into the pre-synaptic neurone- where it is then metabolised
converted to metabolites in the mitochondria by Monoamine oxidase A- MAO-A

Uptake 2- NA taken into the post synaptic neuron- degraded by COMT (Catechol-O-methyltransferase)


Consequence of blocking enzymes that metabolise NA

Increase NA in pre and post-synaptic neurone (reducing conc gradient)- more NA in synapse- less moves back in by transporter