June 15, 2025 • 31 mins
Let’s Get Updated is an audio learning series that brings to life the key topics from Update in Anaesthesia—one topic at a time. Each episode guides you through a full reading of a selected topic, making it easy to listen and read along. Whether you’re preparing for exams or brushing up on essential concepts, this podcast is built for anaesthesia learners in all settings, especially low-resource environments. This is an independent educational project not affiliated with the World Federation of Societies of Anaesthesiologists (WFSA). Content is drawn from publicly available issues of Update in Anaesthesia.
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This episode features a full reading of “The Automatic Nervous System - Basic Anatomy and Physiology” from Update in Anaesthesia, Volume 24, Number 2.
Read along with the original article or simply listen in for a clear, guided walkthrough.
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(00:01):
Updating anaesthesia volume 24 #2 The autonomic nervous system
Basic anatomy and Physiology by Oliver Pratt, Karl ginwood and
Sarah Bakewell summary The autonomic nervous system can be
(00:28):
thought of as the regulatory system that partly or wholly
controls most of the body's organ systems and homeostatic
mechanisms in general. ANS effects are involuntary,
relatively rapid neuronal reflexes.
(00:53):
ANS effects include control of heart rates and force of
contraction, constriction and dilation of blood vessels,
contraction and relaxation of smooth muscle in various organs,
visual accommodation, papillary size, and secretions from
(01:16):
exocrine and endocrine glands. Introduction Many bodily
functions proceed without any conscious supervision from our
central nervous system, CNS. For example, we don't have to
(01:40):
remember to digest our food after a meal or sweat when too
warm. These functions are controlled
subconsciously with a degree of automaticity by a branch of the
nervous system, the autonomic nervous system.
(02:01):
ANS. The ANS is instrumental in the
control of most of the body's organ systems via a series of
neural reflexes. The afferent system.
Sorry. The afferent limb of these
reflexes can be from the peripheral or central nervous
(02:26):
system. The efferent limb is mediated by
the sympathetic or parasympathetic divisions of the
ANS, which are functionally and structurally distinct.
The observed physiological effect of the ANS depends upon
(02:49):
several neurotransmitter and receptor types, and so there are
many targets for pharmacologicalmanipulation.
Afferent pathways, although the ANS is predominantly an efferent
(03:10):
system transmitting impulses from the central nervous system.
CNS to peripheral organ systems.It receives afferent inputs,
that is, transmit information from the periphery to the CNS
into its reflex arcs from the ANS itself.
(03:38):
These afferent neurons are concerned with the mediation of
visceral sensation and the regulation of vasomoto and
respiratory reflexes. Examples are the baroreceptors
and chemoreceptors in the carotid sinus and aortic arc,
(04:01):
which are important in the control of heart rates, blood
pressure and respiratory activity.
The afferent fibres are usually carried to the CNS by major
autonomic nerves such as the vagus, splanknik or pelvic
nerves, although afferent pain fibres from blood vessels may be
(04:25):
carried by somatic nerves other parts of the CNS.
An example is the vessel vagal response to impeding cannulation
in a needle phobic patients Inferent pathways.
(04:51):
The inferent limb of neuronal autonomic reflexes consists of
specific primary autonomic nerves, that is, pre ganglionic
nerves that synapse in autonomicganglia with secondary or post
ganglionic fibres. These post ganglionic fibres
(05:14):
mediate the desired response at the effector organ.
The inferrent limbs of these reflexes may also involve the
somatic nervous system, that is,for example, coughing and
vomiting. Simple reflexes are completed
(05:35):
entirely within the organ concerned, whereas more complex
reflexes are controlled by the higher autonomic centres in the
CNS, principally the hypothalamus.
The effector limb of the ANS is subdivided into two separate
(05:58):
divisions on the basis of anatomical and functional
differences. The sympathetic and
parasympathetic nervous systems.These two divisions differ in
both structure and function. In general, the sympathetic
(06:19):
nervous system can be thought ofas preparing the body for fight
or flight. In the cardiovascular system,
increased ionotropic and chronotropic Dr lead to
increased cardiac output and blood flow is routed towards
vital organs and skeletal muscle.
(06:42):
There is an overall increase in CNS stimulation and respiratory
Dr is increased. Visceral activity is decreased.
The parasympathetic nervous system, in contrast, increases
the activity of the abdominal viscera.
(07:06):
The cardiovascular system is depressed, reducing heart rates
and cardiac outputs and routing blood flow towards visceral
beds. The respiratory system and CNS
are also depressed. Structure of the autonomic
(07:29):
nervous system. Both the sympathetic and
parasympathetic systems consist of myelinated preganglionic
fibres that make synaptic connections with unmyelinated
post ganglionic fibres and it isthese which then innervate the
(07:52):
effector organ. These synapses usually occur in
clusters called ganglia. Most organs are in are
innervated by fibres from both divisions of the ANS and the
influence is usually opposing. For example, the vagus slows the
(08:16):
heart, whilst the sympathetic nerves increase its rate and
contractility. The effects on some organs such
as the salivary glands may be inparallel sympathetic nervous
system. In addition to its close
(08:39):
functional relationship to the central nervous system, the ANS
shares a close anatomical proximity.
In the sympathetic nervous system.
The ganglia are fused to form the sympathetic chain, which
lies adjacent to the spinal column throughout most of its
(09:03):
length. Preganglionic sympathetic fibres
have cell bodies in the intermedial lateral column, that
is the lateral horn of grey matter in the spinal cord
between the first thoracic and 2nd lumbar vertebrae vertebrae
(09:25):
that is T1 to L2. These fibres emerge from the
spinal cord and travel a short distance in the primary ventral
ram Rami of a mixed spinal nervethat is anterior nerve root and
(09:46):
pass to the sympathetic ganglia via the white Rami
communicantis. The ganglia are mainly arranged
in two para vertebral chains, that is the sympathetic
ganglionic chains which lie anterolateral to the vertebral
(10:09):
bodies and extend from the cervical to the sacral region.
In the sympathetic chain the fibres will synapse giving rise
to unmyelinated post ganglionic fibres that rejoin the spinal
nerves via the grey ramen communicantes and are conveyed
(10:34):
to the effector organ. Some pre ganglionic fibres
however, ascend or descend to other levels of the sympathetic
chain prior to synapsin. In general therefore,
(10:55):
sympathetic pre ganglionic fibres are short and post
ganglionic fibres tend to be longer.
Next we get to Figure 1, explaining the anatomy of the
sympathetic nervous system at the spinal level.
(11:18):
Kindly pause this recording to go through Figure 1.
Parasympathetic nervous system. Parasympathetic pre ganglionic
fibres leave the CNS in both cranial and sacral nerves.
(11:43):
Cranial fibres arise from specific parasympathetic brain
stem motonuclei of cranial nerves, three that is oculomotor
nerve, seven that is facial nerve, nine that is
glossopharyngeal nerve and 10 that is vagus nerve.
(12:08):
The fibres travel with the main body of fibres within the
cranial nerves to ganglia that tend to be distant from the CNS
and close to the target organ. The ganglion cells may be either
well organised, for example myenteric plexus of the
(12:31):
intestine, or diffuse, for example the bladder or blood
vessels. In contrast to the sympathetic
nervous system, the pre ganglionic fibres tend to be
long whereas the post ganglionicfibres are shorter.
(12:54):
Sacral pre ganglionic fibres emerge from the CNS via the
ventral Remi of nerves S2 to S4 and form the pelvic splenic
nerves which pass to ganglia close to the infector organs.
(13:17):
The cranial nerves 37 and 9 affect the pupil and salivary
gland secretion, whilst the vagus nerve 10 carries fibres to
the heart, lungs, stomach, upperintestine and ureter.
(13:41):
The sacral fibres form pelvic plexuses, which innovate the
distal colon, rectum, bladder and reproductive organs.
The basic structure of the ANS is illustrated in Figure 2.
(14:02):
Next, we get to Figure 2, talking about the anatomy of the
autonomic nervous system. Kindly pause this recording to
go through Figure 2. The anatomical differences
between the two divisions of theANS have greater clinical
(14:24):
significance, particularly to anaesthetists.
Anaesthetic interventions may have a greater or lesser effect
on the sympathetic or parasympathetic nerves.
A good example of this can be seen during spinal anaesthesia.
(14:49):
A spinal block will temporarily halt inputs to the sympathetic
afferents at the affected levels, leading to vassal
dilatation and loss of sweating in the affected dermatomes.
If the block is allowed to spread to the levels supplying
(15:10):
cardiac sympathetic fibres, thatis, T1 to T4, there will be a
loss of both ionotropic and chronotropic drive to the heart,
reducing the cardiac output and causing progressive hypotension.
The parasympathetic supply to the heart travelling in the
(15:34):
vagus nerve will be unaffected by the spinal block, leading to
unopposed parasympathetic stimulation and bradycardia.
The Physiology of the ANS. In order to understand the
(15:56):
functions of the ANS and the possible targets for
pharmacological manipulation, itis necessary to have a basic
knowledge of the neurotransmitters and receptors
that are integral to the ANS. As with all neuronal systems,
(16:17):
the effects of the ANS and mediated by the release of
neurotransmitters. Preganglionic fibres of both the
sympathetic and parasympathetic nervous systems.
Secret acetylcholine with nicotinic receptors.
(16:37):
See below. Predominating in autonomic
ganglia, sympathetic post ganglionic fibres are mostly
adrenergic in nature. The secret no ethinephrine and
occasionally ethinephrine. Epinephrine and no ethinephrine
(17:03):
are both catecholamines and are both synthesised from the
essential amino acid phenylalanine by a series of
steps which includes the production of dopamine.
The effects of post ganglionic nerve stimulation depends upon
(17:26):
the receptors present at the effector site, usually alpha or
beta adrenoceptors, adreno receptors.
The effects are terminated by noepinephrine rhioptic into the
pre synaptic nerve ending where it is inactivated by the enzyme
(17:50):
monoamine oxidase in mitochondria or metabolism
locally by the enzyme catechol Omethyl transferase.
A special case within the sympathetic nervous system is
the nerve to the adrenal modular.
(18:14):
The adrenal medulla responds to nervous impulses in the
sympathetic cholinergic preganglionic fibres by
transforming the neural impulsesinto hormonal secretion.
This nerve does not synapse within the sympathetic chain and
(18:36):
hence is strictly still preganglionic when it reaches
the adrenal medulla and consequently secrets
acetylcholine as its neurotransmitter.
The cells of the adrenal medullacan be thought of as a modified
(18:56):
autonomic ganglion, but due to the presence of an additional
enzyme the majority of non epinephrine is converted to
epinephrine. In situations involving physical
or physio or psychological stress, much larger quantities
(19:17):
are released. We get to Table 1 explaining
just breaking down a summary of the effects of autonomic nervous
systems at different organs. Very important table.
(19:39):
Kindly pause this recording to go through Table 1.
Parasympathetic post ganglionic fibres release acetylcholine.
Most effects are mediated via muscarinic receptors.
(20:00):
And actions are terminated when acetylcholine is hydrolyzed by
acetylcholinesterase. Within the synaptic cleft,
neurotransmitters bind with specific receptors at Target
cells to produce their effects. Different receptor subtypes
(20:27):
exist in each of the divisions of the ANS, and the
intracellular response in the target cell, and hence the
target organ is specific to the receptor type.
Within the sympathetic nervous system, effects are generally
(20:48):
mediated by adrenal receptors. In the parasympathetic system,
effects are mediated generally by muscarinic acetylcholine
receptors. A further exception to this rule
is the sympathetic post ganglionic fibres supplying
(21:10):
sweat glands. These fibres secrete
acetylcholine and exert their effects via muscarinic
receptors. Adrenal receptors.
(21:31):
Adrenal receptors are subdividedinto alpha and beta receptors.
Each of these classes is furtherdivided into subgroups A1 and
A2, beta 1, beta 2 and beta 3 alpha receptors.
(21:58):
Alpha receptors are G protein linked receptors.
They act via the G protein subgroup GZ and phospholiphase C
to increase cytoplasmic calcium levels.
(22:18):
Next we get to Figure 3, which is a summary of receptor types
and neurotransmitters within theautonomic nervous system.
Very important. Kindly pause this recording to
go through Figure 3. This predominantly leads to
(22:39):
excitatory effects such as smooth muscle contraction.
A1 receptors are widespread in the peripheral vascular tree and
stimulation causes vasoconstriction, increased
systemic vascular resistance, and diversion of blood flow from
(23:03):
the peripheries to the vital organs.
They can further be subdivided into A1 A, A1 B and A1 C based
on receptor structure and agonist response, but at the
(23:23):
moment there is no clinical difference between them within
the ANS. A2 receptors are largely pre
synaptic. They act via the G protein
subgroup GI inhibiting adenylatecyclists, reducing cytoplasmic
(23:51):
cyclic AMP and calcium levels. They may also have a direct
action the activation of potassium channels causing
membrane hyperpolarization. The net effects of these
(24:11):
responses are to down regulate or at least reduce the
sympathetic response. A2 receptors are also present in
parts of the CNS, particularly the Lucas correlius in floor in
(24:31):
the floor of the 4th ventricle. Their function appears to be
linked to the thalamus, reticulospinal tracts, and
vasomotocentre, with activation causing analgesia, drowsiness,
and hypertension. A2 receptors can also be
(24:56):
subdivided into four further subtypes.
Beta receptors. Beta receptors are again G
protein linked receptors. Stimulation leads to increase
(25:18):
activity of adenylate cyclase that in turn increases
intracellular cyclic AMP. There are three major subgroups
of beta receptors, beta 1, beta 2 and beta 3 and recently 1/4
(25:42):
has been described but as yet itis not setting of its exact
function. Beta one and beta 4 receptors
predominate in the heart, that is about 85%.
But the traditional view that beta one are cardiac and beta 2
(26:04):
are peripheral is probably an oversimplification.
The beta receptor population is rather fluid in nature.
Receptors can be down or up regulated in terms of number and
function. A good example of this is seen
(26:28):
in cardiac failure where reducedreceptor density is observed in
cardiac muscle. Clinically, beta one receptor
stimulation leads to increased heart rate and positive
ionotrophy. Renin release from the
(26:51):
juxtaglomerular apparatus is stimulated leading to activation
of the renin angiotensin aldosterone axis.
Beta 2 receptor stimulation causes relaxation of bronchial
and uterine smooth muscle, vasodilatation in some vascular
(27:16):
beds, for example, skeletal muscle, pulmonary, coronary, and
some degree of positive ionotrophy and chronotrophy.
Beta 3 receptors are found in adipose tissue and have a role
(27:37):
in regulating metabolism, thermogenesis, and body fat.
Acetylcholine Receptors Acetylcholine receptors are
named according to The Agonist that they respond to
(27:59):
experimentally. Those activated by nicotine are
termed nicotinic receptors, whereas those that are that are
responded to muscarin are named muscarinic receptors.
(28:20):
Nicotinic Receptors Nicotinic receptors are ion channels that,
when stimulated by acetylcholine, allow a flow of
cations into the cell, causing depolarization.
(28:40):
They are found in all autonomic ganglia.
Acetylcholine receptors at the motor end plates of the
neuromuscular junction are historically nicotinic, but
their structure differs slightlyfrom those of the ANS muscarinic
(29:05):
receptors. Muscarinic receptors mediate the
majority of effects caused by parasympathetic post ganglionic
fibres. Like adeno receptors, they are G
protein linked receptors and arefurther divided by structure and
(29:28):
location into subtypes M1 to M5.M1 receptors are found on
gastric parietal cells and stimulate acid secretion.
M2 receptors are found in the heart and have negatively
(29:52):
chronatrophic effects. M3 receptors promote smooth
muscle contraction in the gut and promote lacrimal secretion.
M4 receptors cause adrenaline release from the adrenal medulla
(30:12):
in response to sympathetic stimulation and M5 receptors are
thought to have CNS effects. Summary The autonomic nervous
system controls non voluntary bodily functions in a reflex arc
(30:38):
with afferent signals being processed either locally or in
the brainstem. Its function and dysfunction are
important to anaesthetists in that many of the drugs used in
anaesthesia and intensive care are used to specifically
modulate autonomic receptors in the control of the cardio,
(31:02):
respiratory and neurologic systems.
Other drugs have unwanted autonomic side effects which
need to be treated, such as using an anticholinergic.
When reversing neuromuscular blockade.
We must take into account the autonomic dysfunction seen in
(31:27):
such widespread scenarios as diabetes, Gullion Barre syndrome
and tricyclic antidepressant overdose, and we must also be
aware of the normal dysautonomiaseen with old age, as this can
(31:49):
exaggerate the effects of many anaesthetic agents and
techniques.
Updating anaesthesia volume 24 #2 The autonomic nervous system
Basic anatomy and Physiology by Oliver Pratt, Karl ginwood and
Sarah Bakewell summary The autonomic nervous system can be
(00:28):
thought of as the regulatory system that partly or wholly
controls most of the body's organ systems and homeostatic
mechanisms in general. ANS effects are involuntary,
relatively rapid neuronal reflexes.
(00:53):
ANS effects include control of heart rates and force of
contraction, constriction and dilation of blood vessels,
contraction and relaxation of smooth muscle in various organs,
visual accommodation, papillary size, and secretions from
(01:16):
exocrine and endocrine glands. Introduction Many bodily
functions proceed without any conscious supervision from our
central nervous system, CNS. For example, we don't have to
(01:40):
remember to digest our food after a meal or sweat when too
warm. These functions are controlled
subconsciously with a degree of automaticity by a branch of the
nervous system, the autonomic nervous system.
(02:01):
ANS. The ANS is instrumental in the
control of most of the body's organ systems via a series of
neural reflexes. The afferent system.
Sorry. The afferent limb of these
reflexes can be from the peripheral or central nervous
(02:26):
system. The efferent limb is mediated by
the sympathetic or parasympathetic divisions of the
ANS, which are functionally and structurally distinct.
The observed physiological effect of the ANS depends upon
(02:49):
several neurotransmitter and receptor types, and so there are
many targets for pharmacologicalmanipulation.
Afferent pathways, although the ANS is predominantly an efferent
(03:10):
system transmitting impulses from the central nervous system.
CNS to peripheral organ systems.It receives afferent inputs,
that is, transmit information from the periphery to the CNS
into its reflex arcs from the ANS itself.
(03:38):
These afferent neurons are concerned with the mediation of
visceral sensation and the regulation of vasomoto and
respiratory reflexes. Examples are the baroreceptors
and chemoreceptors in the carotid sinus and aortic arc,
(04:01):
which are important in the control of heart rates, blood
pressure and respiratory activity.
The afferent fibres are usually carried to the CNS by major
autonomic nerves such as the vagus, splanknik or pelvic
nerves, although afferent pain fibres from blood vessels may be
(04:25):
carried by somatic nerves other parts of the CNS.
An example is the vessel vagal response to impeding cannulation
in a needle phobic patients Inferent pathways.
(04:51):
The inferent limb of neuronal autonomic reflexes consists of
specific primary autonomic nerves, that is, pre ganglionic
nerves that synapse in autonomicganglia with secondary or post
ganglionic fibres. These post ganglionic fibres
(05:14):
mediate the desired response at the effector organ.
The inferrent limbs of these reflexes may also involve the
somatic nervous system, that is,for example, coughing and
vomiting. Simple reflexes are completed
(05:35):
entirely within the organ concerned, whereas more complex
reflexes are controlled by the higher autonomic centres in the
CNS, principally the hypothalamus.
The effector limb of the ANS is subdivided into two separate
(05:58):
divisions on the basis of anatomical and functional
differences. The sympathetic and
parasympathetic nervous systems.These two divisions differ in
both structure and function. In general, the sympathetic
(06:19):
nervous system can be thought ofas preparing the body for fight
or flight. In the cardiovascular system,
increased ionotropic and chronotropic Dr lead to
increased cardiac output and blood flow is routed towards
vital organs and skeletal muscle.
(06:42):
There is an overall increase in CNS stimulation and respiratory
Dr is increased. Visceral activity is decreased.
The parasympathetic nervous system, in contrast, increases
the activity of the abdominal viscera.
(07:06):
The cardiovascular system is depressed, reducing heart rates
and cardiac outputs and routing blood flow towards visceral
beds. The respiratory system and CNS
are also depressed. Structure of the autonomic
(07:29):
nervous system. Both the sympathetic and
parasympathetic systems consist of myelinated preganglionic
fibres that make synaptic connections with unmyelinated
post ganglionic fibres and it isthese which then innervate the
(07:52):
effector organ. These synapses usually occur in
clusters called ganglia. Most organs are in are
innervated by fibres from both divisions of the ANS and the
influence is usually opposing. For example, the vagus slows the
(08:16):
heart, whilst the sympathetic nerves increase its rate and
contractility. The effects on some organs such
as the salivary glands may be inparallel sympathetic nervous
system. In addition to its close
(08:39):
functional relationship to the central nervous system, the ANS
shares a close anatomical proximity.
In the sympathetic nervous system.
The ganglia are fused to form the sympathetic chain, which
lies adjacent to the spinal column throughout most of its
(09:03):
length. Preganglionic sympathetic fibres
have cell bodies in the intermedial lateral column, that
is the lateral horn of grey matter in the spinal cord
between the first thoracic and 2nd lumbar vertebrae vertebrae
(09:25):
that is T1 to L2. These fibres emerge from the
spinal cord and travel a short distance in the primary ventral
ram Rami of a mixed spinal nervethat is anterior nerve root and
(09:46):
pass to the sympathetic ganglia via the white Rami
communicantis. The ganglia are mainly arranged
in two para vertebral chains, that is the sympathetic
ganglionic chains which lie anterolateral to the vertebral
(10:09):
bodies and extend from the cervical to the sacral region.
In the sympathetic chain the fibres will synapse giving rise
to unmyelinated post ganglionic fibres that rejoin the spinal
nerves via the grey ramen communicantes and are conveyed
(10:34):
to the effector organ. Some pre ganglionic fibres
however, ascend or descend to other levels of the sympathetic
chain prior to synapsin. In general therefore,
(10:55):
sympathetic pre ganglionic fibres are short and post
ganglionic fibres tend to be longer.
Next we get to Figure 1, explaining the anatomy of the
sympathetic nervous system at the spinal level.
(11:18):
Kindly pause this recording to go through Figure 1.
Parasympathetic nervous system. Parasympathetic pre ganglionic
fibres leave the CNS in both cranial and sacral nerves.
(11:43):
Cranial fibres arise from specific parasympathetic brain
stem motonuclei of cranial nerves, three that is oculomotor
nerve, seven that is facial nerve, nine that is
glossopharyngeal nerve and 10 that is vagus nerve.
(12:08):
The fibres travel with the main body of fibres within the
cranial nerves to ganglia that tend to be distant from the CNS
and close to the target organ. The ganglion cells may be either
well organised, for example myenteric plexus of the
(12:31):
intestine, or diffuse, for example the bladder or blood
vessels. In contrast to the sympathetic
nervous system, the pre ganglionic fibres tend to be
long whereas the post ganglionicfibres are shorter.
(12:54):
Sacral pre ganglionic fibres emerge from the CNS via the
ventral Remi of nerves S2 to S4 and form the pelvic splenic
nerves which pass to ganglia close to the infector organs.
(13:17):
The cranial nerves 37 and 9 affect the pupil and salivary
gland secretion, whilst the vagus nerve 10 carries fibres to
the heart, lungs, stomach, upperintestine and ureter.
(13:41):
The sacral fibres form pelvic plexuses, which innovate the
distal colon, rectum, bladder and reproductive organs.
The basic structure of the ANS is illustrated in Figure 2.
(14:02):
Next, we get to Figure 2, talking about the anatomy of the
autonomic nervous system. Kindly pause this recording to
go through Figure 2. The anatomical differences
between the two divisions of theANS have greater clinical
(14:24):
significance, particularly to anaesthetists.
Anaesthetic interventions may have a greater or lesser effect
on the sympathetic or parasympathetic nerves.
A good example of this can be seen during spinal anaesthesia.
(14:49):
A spinal block will temporarily halt inputs to the sympathetic
afferents at the affected levels, leading to vassal
dilatation and loss of sweating in the affected dermatomes.
If the block is allowed to spread to the levels supplying
(15:10):
cardiac sympathetic fibres, thatis, T1 to T4, there will be a
loss of both ionotropic and chronotropic drive to the heart,
reducing the cardiac output and causing progressive hypotension.
The parasympathetic supply to the heart travelling in the
(15:34):
vagus nerve will be unaffected by the spinal block, leading to
unopposed parasympathetic stimulation and bradycardia.
The Physiology of the ANS. In order to understand the
(15:56):
functions of the ANS and the possible targets for
pharmacological manipulation, itis necessary to have a basic
knowledge of the neurotransmitters and receptors
that are integral to the ANS. As with all neuronal systems,
(16:17):
the effects of the ANS and mediated by the release of
neurotransmitters. Preganglionic fibres of both the
sympathetic and parasympathetic nervous systems.
Secret acetylcholine with nicotinic receptors.
(16:37):
See below. Predominating in autonomic
ganglia, sympathetic post ganglionic fibres are mostly
adrenergic in nature. The secret no ethinephrine and
occasionally ethinephrine. Epinephrine and no ethinephrine
(17:03):
are both catecholamines and are both synthesised from the
essential amino acid phenylalanine by a series of
steps which includes the production of dopamine.
The effects of post ganglionic nerve stimulation depends upon
(17:26):
the receptors present at the effector site, usually alpha or
beta adrenoceptors, adreno receptors.
The effects are terminated by noepinephrine rhioptic into the
pre synaptic nerve ending where it is inactivated by the enzyme
(17:50):
monoamine oxidase in mitochondria or metabolism
locally by the enzyme catechol Omethyl transferase.
A special case within the sympathetic nervous system is
the nerve to the adrenal modular.
(18:14):
The adrenal medulla responds to nervous impulses in the
sympathetic cholinergic preganglionic fibres by
transforming the neural impulsesinto hormonal secretion.
This nerve does not synapse within the sympathetic chain and
(18:36):
hence is strictly still preganglionic when it reaches
the adrenal medulla and consequently secrets
acetylcholine as its neurotransmitter.
The cells of the adrenal medullacan be thought of as a modified
(18:56):
autonomic ganglion, but due to the presence of an additional
enzyme the majority of non epinephrine is converted to
epinephrine. In situations involving physical
or physio or psychological stress, much larger quantities
(19:17):
are released. We get to Table 1 explaining
just breaking down a summary of the effects of autonomic nervous
systems at different organs. Very important table.
(19:39):
Kindly pause this recording to go through Table 1.
Parasympathetic post ganglionic fibres release acetylcholine.
Most effects are mediated via muscarinic receptors.
(20:00):
And actions are terminated when acetylcholine is hydrolyzed by
acetylcholinesterase. Within the synaptic cleft,
neurotransmitters bind with specific receptors at Target
cells to produce their effects. Different receptor subtypes
(20:27):
exist in each of the divisions of the ANS, and the
intracellular response in the target cell, and hence the
target organ is specific to the receptor type.
Within the sympathetic nervous system, effects are generally
(20:48):
mediated by adrenal receptors. In the parasympathetic system,
effects are mediated generally by muscarinic acetylcholine
receptors. A further exception to this rule
is the sympathetic post ganglionic fibres supplying
(21:10):
sweat glands. These fibres secrete
acetylcholine and exert their effects via muscarinic
receptors. Adrenal receptors.
(21:31):
Adrenal receptors are subdividedinto alpha and beta receptors.
Each of these classes is furtherdivided into subgroups A1 and
A2, beta 1, beta 2 and beta 3 alpha receptors.
(21:58):
Alpha receptors are G protein linked receptors.
They act via the G protein subgroup GZ and phospholiphase C
to increase cytoplasmic calcium levels.
(22:18):
Next we get to Figure 3, which is a summary of receptor types
and neurotransmitters within theautonomic nervous system.
Very important. Kindly pause this recording to
go through Figure 3. This predominantly leads to
(22:39):
excitatory effects such as smooth muscle contraction.
A1 receptors are widespread in the peripheral vascular tree and
stimulation causes vasoconstriction, increased
systemic vascular resistance, and diversion of blood flow from
(23:03):
the peripheries to the vital organs.
They can further be subdivided into A1 A, A1 B and A1 C based
on receptor structure and agonist response, but at the
(23:23):
moment there is no clinical difference between them within
the ANS. A2 receptors are largely pre
synaptic. They act via the G protein
subgroup GI inhibiting adenylatecyclists, reducing cytoplasmic
(23:51):
cyclic AMP and calcium levels. They may also have a direct
action the activation of potassium channels causing
membrane hyperpolarization. The net effects of these
(24:11):
responses are to down regulate or at least reduce the
sympathetic response. A2 receptors are also present in
parts of the CNS, particularly the Lucas correlius in floor in
(24:31):
the floor of the 4th ventricle. Their function appears to be
linked to the thalamus, reticulospinal tracts, and
vasomotocentre, with activation causing analgesia, drowsiness,
and hypertension. A2 receptors can also be
(24:56):
subdivided into four further subtypes.
Beta receptors. Beta receptors are again G
protein linked receptors. Stimulation leads to increase
(25:18):
activity of adenylate cyclase that in turn increases
intracellular cyclic AMP. There are three major subgroups
of beta receptors, beta 1, beta 2 and beta 3 and recently 1/4
(25:42):
has been described but as yet itis not setting of its exact
function. Beta one and beta 4 receptors
predominate in the heart, that is about 85%.
But the traditional view that beta one are cardiac and beta 2
(26:04):
are peripheral is probably an oversimplification.
The beta receptor population is rather fluid in nature.
Receptors can be down or up regulated in terms of number and
function. A good example of this is seen
(26:28):
in cardiac failure where reducedreceptor density is observed in
cardiac muscle. Clinically, beta one receptor
stimulation leads to increased heart rate and positive
ionotrophy. Renin release from the
(26:51):
juxtaglomerular apparatus is stimulated leading to activation
of the renin angiotensin aldosterone axis.
Beta 2 receptor stimulation causes relaxation of bronchial
and uterine smooth muscle, vasodilatation in some vascular
(27:16):
beds, for example, skeletal muscle, pulmonary, coronary, and
some degree of positive ionotrophy and chronotrophy.
Beta 3 receptors are found in adipose tissue and have a role
(27:37):
in regulating metabolism, thermogenesis, and body fat.
Acetylcholine Receptors Acetylcholine receptors are
named according to The Agonist that they respond to
(27:59):
experimentally. Those activated by nicotine are
termed nicotinic receptors, whereas those that are that are
responded to muscarin are named muscarinic receptors.
(28:20):
Nicotinic Receptors Nicotinic receptors are ion channels that,
when stimulated by acetylcholine, allow a flow of
cations into the cell, causing depolarization.
(28:40):
They are found in all autonomic ganglia.
Acetylcholine receptors at the motor end plates of the
neuromuscular junction are historically nicotinic, but
their structure differs slightlyfrom those of the ANS muscarinic
(29:05):
receptors. Muscarinic receptors mediate the
majority of effects caused by parasympathetic post ganglionic
fibres. Like adeno receptors, they are G
protein linked receptors and arefurther divided by structure and
(29:28):
location into subtypes M1 to M5.M1 receptors are found on
gastric parietal cells and stimulate acid secretion.
M2 receptors are found in the heart and have negatively
(29:52):
chronatrophic effects. M3 receptors promote smooth
muscle contraction in the gut and promote lacrimal secretion.
M4 receptors cause adrenaline release from the adrenal medulla
(30:12):
in response to sympathetic stimulation and M5 receptors are
thought to have CNS effects. Summary The autonomic nervous
system controls non voluntary bodily functions in a reflex arc
(30:38):
with afferent signals being processed either locally or in
the brainstem. Its function and dysfunction are
important to anaesthetists in that many of the drugs used in
anaesthesia and intensive care are used to specifically
modulate autonomic receptors in the control of the cardio,
(31:02):
respiratory and neurologic systems.
Other drugs have unwanted autonomic side effects which
need to be treated, such as using an anticholinergic.
When reversing neuromuscular blockade.
We must take into account the autonomic dysfunction seen in
(31:27):
such widespread scenarios as diabetes, Gullion Barre syndrome
and tricyclic antidepressant overdose, and we must also be
aware of the normal dysautonomiaseen with old age, as this can
(31:49):
exaggerate the effects of many anaesthetic agents and
techniques.
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