physiology of Autonomic nervous system

1
Maninder Kaur M.Pharm (Pharmacology)

 The autonomic nervous system is the subdivision
of the peripheral nervous system that regulates
body activities that are generally not under
conscious control
 Visceral motor innervates non-skeletal (non-
somatic) muscles
 Visceral sensory will be covered later
2Maninder Kaur M.Pharm (Pharmacology)

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Diagram of Autonomic nervous system
Diagram contrasts somatic (lower) and autonomic:
autonomic
somatic
this dorsal
root ganglion
is sensory

 Neurotransmission in ANS occurs in 5 steps:
• Impulse conduction.
• Neurotransmitter release.
• Activity on preganglionic neurons.
• Activity on postganglionic neurons.
• Termination of neurotransmitter release.
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 Parasympathetic division
 Sympathetic division
Parasympathetic: routine maintenance.
“rest &digest”
Sympathetic: mobilization & increased
metabolism.
“fight, flight or fright”

2 divisions:
 Sympathetic
▪ “Fight or flight”
▪ “E” division
▪ Exercise, excitement,
emergency, and
embarrassment
 Parasympathetic
▪ “Rest and digest”
▪ “D” division
▪ Digestion, defecation,
and diuresis

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 Also called the craniosacral system because
all its preganglionic neurons are in the brain
stem or sacral levels of the spinal cord.
 Cranial nerves III,VII, IX and X
 In lateral horn of gray matter from S2-S4
 Only innervate internal organs (not skin).
 Acetylcholine is neurotransmitter at end
organ as well as at preganglionic synapse:
“cholinergic”.

 Works to save energy, aids in digestion, and
supports restorative, resting body functions.
 Decrease in heart rate
 Increased gastro intestinal tract tone and
peristalsis
 Urinary sphincter relaxation
 Vasodilation – decrease in blood pressure

Location of cholinergic receptors-
1. Postganglionic parasympathetic neuroeffector junctions.
2. All autonomic ganglia.
3. At the neuromuscular endplate.

Two types of receptors are present-
 Muscarinic receptor.
 Nicotinic receptor.

M-cholinoceptors can be classified into subtypes
according to their molecular structure, signal
transduction, and ligand affinity in the M1, M2, M3
subtypes etc.
• M1-receptors are present on nerve cells, e.g., in
ganglia, where they mediate a facilitation of impulse
transmission from preganglionic axon terminals to
ganglion cells.
• M2-receptors mediate acetylcholine effects on the
heart. Opening of K+
channels leads to slowing of
diastolic depolarization in sinoatrial pacemaker cells
and a decrease in heart rate. 16Maninder Kaur M.Pharm (Pharmacology)

M3-receptors are found in the glandular epithelia
(which respond with activation of phospholipase
C and increases secretory activity) and in smooth
muscle.
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Muscarinic receptor (G protein-linked: 7 subunits)
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NM -cholinoceptors
Location: neuromuscular junction.
Function: depolarization of muscle end
plate and contraction of skeletal muscle.
NN -cholinoceptors
Location: autonomic ganglia.
Function: depolarization
postganglionic membrane (in adrenal medulla –
catecholamine release).

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(1) Choline ester (stimulants of M- and N-
receptors):
 Acetylcholine, Carbachol, etc.
(2) Alkaloids
 a) stimulants of M-receptors:
▪ Pilocarpine, Cevimeline (dry mouth),
▪ Bethanechole, Musacarine, Phalloidin
 b) stimulants of N-receptors:
▪ Nicotine, Cytisine (Tabex®
), Lobeline

(1) Reversible drugs (most are carbamates)
a) With N3+
(cross BBB)
Alkaloids: Galantamine, Physostigmine
Synthetic drugs: Donepezil, Rivastigmine,
Tacrine.
b) With N4+
(do not cross BBB)- Demecarium,
Edrophonium (Tensilon®
),Neostigmine,
Pyridostigmine.

(2) Irreversible anticholinesterase agents (most of
them are organophosphates)-
a) Thiophosphate insecticides
 Parathion
 Malathion (Pedilin®
– in pediculosis)
b) Nerve paralytic gases for chemical warfare
 Tabun
 Sarin
 Soman

 cardiac output M2: decreases
 SA node: heart rate (chronotropic) M2: decreases
 cardiac muscle: contractility (inotropic) M2: decreases (atria only)
 conduction at AV node M2: decreases
 smooth muscles of bronchioles M3: contracts
 pupil of eye M3: contracts
 ciliary muscle M3: contracts
 salivary glands: secretions stimulates watery secretions
 GI tract motility M1, M3: increases
 smooth muscles of GI tract M3: contracts
 sphincters of GI tract M3: relaxes
 glands of GI tract M3: secretes

 Myasthenia gravis.
 Belladonna poisoning.
 In glucoma

 These are drugs which oppose the
acetylcholine actions or block the cholinergic
receptors.
 Anti- cholinergics mainly block the
muscarinic receptor.

 Atropine, the prototype drug of this class, is a
highly selective blocking agent for pre and post
muscarinic receptors, but some of its synthetic
derivatives have significant nicotinic blocking
property as well.

1. Natural alkaloids: Atropine (spasmolytic, mydriatic),
 Hyoscine (Scopolamine), Scopoderm®
TTS (antiemetic)
2. Semisynthetic derivatives
• Mydriatics: Homatropine
• GI spasmolytics: Hyoscine butyl bromide (Buscolysin®
)

3. Synthetic compounds
• GI spasmolytics: Oxyphenonium
• Antiulcus drugs: Pirenzepine (M1-blockers)
• Antiasthmatics: Ipratropium and Tiotropium
• Antidisurics: Flavoxate, Oxybutynyne, Trospium
• Mydriatics: Tropicamide
• Antiparkinsonian (central M-cholinolytics):
▪ Benztropine, Biperiden, Trihexyphenidyl

Atropine
(-)

• CNS. Atropine has an overall stimulant action. Its
stimulant effects are not appreciable at low doses which
produce peripheral effects because of restricted entry into
the brain.
• Atropine stimulates many medullar centers- vagal,
respiratory, and vasоmotor.
• By blocking the relative cholinergic overactivity in basal
ganglia, it suppresses tremor and rigidity in
parkinsonism.
• High doses cause cortical excitation, rest- lessness,
disorientation, hallucinations.

 CVS. Atropine causes tachycardia, due to blockade of M2-
receptors on SA node through which vagal tone decreases
HR.
 Atropine does not influence BP. It blocks the
vasodepressor action of cholinergic agonists.
 Eye. Topical instillation of atropine (0.1%) causes
mydriasis, abolition of light reflex, and cycloplegia, lasting
7–10 days. This results in photophobia and blurring of near
vision. The intraocular tension rises, specially in narrow
angle glaucoma, but conventional systemic doses produce
minor ocular effects.

 Smooth muscles. All visceral smooth muscles with
parasympathetic inervation are relaxed (M3 blokade).Tone
and amplitude of GIT are reduced. Spasm may be
reduced, constipation may occur. Peristalsis is only
incompletely suppressed because it is primarily regulated
by local reflexes and other neurotransmitters (serotonin,
encephalin, etc.).
 Atropine causes bronchodilation and reduced airway
resistance, especially in asthma patients.

 Glands. Atropine decreases sweat, salivary, tracheo-
bronchial, and lacrimal secretion (M3-blockade). Skin and
eyes become dry, talking, and swallowing my be very
difficult. Atropine decreases less the secretion of acid and
pep-sin and more of the mucus in the stomach.
 Body temperature. Rise in body temperature occurs at
higher doses, and is due to both inhibition of sweating as
well as stimulation of the temperature regulating centre in
the hypothalamus.

saliva, sweat, bronchial secretion > eye >
bronchial muscles > heart > intestinal and
bladder smooth muscles > gastric glands
and gastric smooth muscles

NEUROMUSCULAR BLOCKING AGENTS:
Skeletal muscle relaxants act peripherally at neuromuscular
junction. According to their action they are divided into the
following groups.
•Nondepolarizing (competitive) agents or curare-like drugs
•Depolarizing (hyperdepolarazing) agents

 Also called thoracolumbar system: all its neurons
are in lateral horn of gray matter from T1-L2
 Lead to every part of the body
 Easy to remember that when nervous, you sweat; when
afraid, hair stands on end; when excited blood pressure
rises (vasoconstriction): these sympathetic only
 Also causes: dry mouth, pupils to dilate, increased heart &
respiratory rates to increase O2 to skeletal muscles, and
liver to release glucose
 Norepinephrine (noradrenaline) is neurotransmitter
released by most postganglionic fibers
(acetylcholine in preganglionic): “adrenergic”

 Helps the body cope with external stimuli and
functions during stress (triggers the flight or
fight response)
 Vasoconstriction – increase in blood pressure
 Increased heart rate
 Increased respiratory rate
 Cold, sweaty palms
 Pupil dilation

 Sympathetic and parasympathetic divisions typically
function in opposition to each other. But this opposition is
better termed complementary in nature rather than
antagonistic. For an analogy, one may think of the
sympathetic division as the accelerator and the
parasympathetic division as the brake. The sympathetic
division typically functions in actions requiring quick
responses. The parasympathetic division functions with
actions that do not require immediate reaction. Consider
sympathetic as "fight or flight" and parasympathetic as "rest
and digest".

physiology of Autonomic nervous system

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