2. • The autonomic nervous system (ANS) is a division
of the peripheral nervous system that influences
the function of internal organs.
• The autonomic nervous system is a control
system that acts largely unconsciously and
regulates bodily functions such as the heart rate,
digestion, respiratory rate, pupillary response,
urination, and sexual arousal.
• This system is the primary mechanism in control
of the fight-or-flight response and the freeze-and-
dissociate response.
3. • The autonomic nervous system has two branches: the sympathetic
nervous system and the parasympathetic nervous system.
• The sympathetic nervous system is often considered the "fight or
flight" system, while the parasympathetic nervous system is often
considered the "rest and digest" or "feed and breed" system.
• In many cases, both of these systems have "opposite" actions
where one system activates a physiological response and the other
inhibits it.
• An older simplification of the sympathetic and parasympathetic
nervous systems as "excitory" and "inhibitory" was overturned due
to the many exceptions found
4. Differences between Autonomic and Somatic Nerves
• The Ans system supply all innervated structures of the body except
skeletal muscle, which is served by somatic nerves.
• The most distal synaptic junctions in the autonomic reflex arc occur in
ganglia that are entirely outside the cerebrospinal axis. Somatic nerves
contain no peripheral ganglia
• Many autonomic nerves form extensive peripheral plexuses, but such
networks are absent from the somatic system.
• Whereas motor nerves to skeletal muscles(somatic ) are myelinated,
postganglionic autonomic nerves generally are nonmyelinated.
• When the spinal efferent nerves are interrupted, the denervated skeletal
muscles (somatic) lack myogenic tone, are paralyzed, and atrophy,
whereas smooth muscles and glands(ANS) generally retain some level of
spontaneous activity independent of intact innervation.
• Efferent neurostransmitter-Ach in somatic, both Ach and Adr in ANS
5. The ANS has two major portions:
the sympathetic (thoracolumbar) division and
the parasympathetic (craniosacral) division.
Both divisions originate in the CNS and give rise to
preganglionic efferent fibers that exit from the brain
stem or spinal cord and terminate in motor ganglia.
The sympathetic preganglionic fibers leave the
CNS through the thoracic and lumbar spinal nerves.
The parasympathetic preganglionic fibers leave the
CNS through the cranial nerves (especially the third,
seventh, ninth, and tenth) and the third and fourth
sacral spinal roots.
6.
7. • Most blood vessels, spleen, sweat glands and
hair follicles receive only sympathetic supply,
• Whereas ciliary muscle, gastric gland and
pancreatic glands receive only
parasympathetic supply.
8. Sympathetic Parasympathetic
• Origin Dorsolumbar(T1 to L2 ) Craniosacral (3,7,9,10.s2-s4)
• Distrubution. Wide Limited to head, neck and trunk.
• Ganglia Away from organs Close to organs
• Post ganglionic fibres. Long Short.
• Pre : Post ganglionic fibre ratio. 1:20 1:1 or 1:2
• Transmitter NA- Nor adrenaline(Major), Acetylcholine(Ach)
Ach(minor)
• Stability of transmitter. NA stable Ach-destroyed rapidly
• Important function. Tackling stress and emergency Assimilation of food,
conserves energy.
9. • Parasympathetic nerves regulate processes connected with energy
assimilation (food intake,digestion, absorption) and storage.
• These processes operate when the body is at rest, allowing increased
bronchomotor toneand decreased cardiac activity.
• Secretion of saliva and intestinal fluids promotes the digestion of
foodstuffs; transport of intestinal contents is speeded up because of
enhanced peristaltic activityand lowered tone of sphincter muscles.
• To empty the urinary bladder (micturition), wall tension is increased by
detrusor activation with a concurrent relaxation of sphincter tonus.
10. • Activation of ocular parasympathetic fibers
results in narrowing of the pupil and increased
curva-ture of the lens, enabling near objects
to be brought into focus (accommodation).
11. Sympathetic nervous system
• Promotes a fight-or-flight response, corresponds with arousal and energy
generation, and inhibits digestion
• Diverts blood flow away from the gastro-intestinal (GI) tract and skin via
vasoconstriction
• Blood flow to skeletal muscles and the lungs is enhanced
• Dilates bronchioles of the lung
• Increases heart rate and the contractility of cardiac cells myocytes, thereby
providing a mechanism for enhanced blood flow to skeletal muscles
• Dilates pupils and relaxes the ciliary muscle to the lens, allowing more light to
enter the eye and far vision
• Provides vasodilation for the coronary vessels of the heart
• Constricts all the intestinal sphincters and the urinary sphincter
• Inhibits peristalsis
• Stimulates orgasm
12. Neurohumoral transmission
It is a process by which a presynaptic cell, on
excitation, releases a specific chemical agent
(a neurotransmitter) to cross a synapse to
stimulate or inhibit the postsynaptic cell.
13. Steps involved in neurohumoral
transmission.
• Impulse conduction.
• Transmitter release
• Transmitter action on postjunctional
membrane
• Postjunctional activity
• Termination of transmitter action
14. 1.Impulse conduction
-70 mv inside
Na is extracellular and K is intracellular
Na moves in and K out- depolarisation
Na and K becomes normal in sodium and
potassium pump
15. 2.Transmitter release
By synaptic vesicles--- calcium entry which
fluidises membrane and releases enzymes,
proteins by exocytosis.
3. Transmitter action on postjunctional
membrane:
EPSP- Sosium or calcium influx and Potassium
efflux
IPSP-Potassium efflux and chloride ion influx
16. 4. Postjunctional activity
EPSP results in nerve impulse in neurons,
contraction in muscle or secretion in gland
5. Termination of transmitter action
Ach is locally degraded
NA, GABA is actively uptaken or diffuses away
18. Cholinergic transmission.
• Synthesis of Ach
ATP+ Acetate+CoEn A
Acetate activating reaction
Acetyl Co-A
Choline acetylase
choline
Acetylcholine + Co-En A
19.
20. • Acetylcholinesterase- present in all cholinergic sites,
RBC, grey matter
Butryl cholinesterase- Present plasma, intestine, liver
and white matter
• Acetylcholinesterase-Hydrolsis(Ach)- Fast
Butryl cholinesterase- Ach -Slow
• Acetylcholinesterase-Inhibited by Physostigmine
Butryl cholinesterase- By Organophosphates
• Acetylcholinesterase-Function- Termination of
transmitter action.
Butryl cholinesterase-Hydrolysis of ingested esters
21. CHOLINERGIC RECEPTORS
M1-Autonomic ganglia- Depolarisation
Gastric glands-Acid secretion
CNS-Not known.
ACTS BY IP3 DAG MECHANISM INCRESING CYTOSOLIC CALCIUM ALL ARE G PROTEIN COUPLED RECEPTORS
Agonist: Oxotremorine
Antagonist: Pirenzepine, Telenzepine
M2-
SA node- decreased impulse
AV node- Increased velocity
Atrium- Decreased contractility.
Ventricle- Decreased contractility
Cholinergic nerve endings- Decreased Ach release.
ACTS BY POTASSIUM CHANNEL OPENING AND DECREASING cAMP MECHANISM
Agonist: Methacholine
Antagonist: Methoctramine, Triptamine
M3-
Visceral smooth muscle- Contraction
Exocrine glands- Secretion
Vascular endothelium- Release of NO and vasodilation
ACTS BY IP3 DAG MECHANISM INCRESING CYTOSOLIC CALCIUM
Agonist: Bethanechol
Antagonist: Darifenacin
22. • NM
Neuromuscular junction- Depolarisation of muscle end plate
Contraction of sketelal muscle
• ACTS BY POTASSIUM OR SODIUM CHANNEL OPENING
Agonist: Nicotine
Antagonist: Tubocurarine
The mAChRs are not ion channels, but belong instead to the superfamily of G-protein-
coupled receptors that activate other ionic channels via a second messenger cascade
NN
Autonomic ganglia: Depolarisation-Postganglionic impulse
Adrenal medulla- Catecholamine release
CNS- Site specific excitation or inhibition
• ACTS BY POTASSIUM OR SODIUM OR CALCIUM CHANNEL OPENING
Agonist: Nicotine
Antagonist: Hexamethonium
The nAChRs are ligand-gated ion channel
23. Cholinergic drugs(Cholinomimetic,
Parasympathomimetic)
• These are drugs which produce actions similar to acetylcholine. These are also called as
cholinomimetic drugs or parasympathomimetic drugs
Classification oF cholinergic agonists
• Choline esters: Acetylcholine, methacholine, carbachol, bethanechol.
• Alkaloids: Muscarine, Pilocarine, Arecoline.
Pharmacology of acetylcholine
• Muscarinic actions
• Heart Acetylcholine causes bradycardia, Force of atrial contraction is reduced
• Blood vessels. Vasodilation and causes fall in b.p
• Smooth muscle: Tone and peristalsis in git is increased. Helps in emptying of bladder, causes
bronchial muscle constriction.
• Glands: Glands are stimulated and it causes salivation and sweating, lacrymation.
• Eye: It cause miosis (Contraction of circular muscle of iris)
24. • Nicotinic actions:
• Autonomic ganglia: Both sympathetic and parasympathetic gangla
are stimulated.
• Skeletal muscles: It causes twitching of fibres and fasiculations.
• CNS: Direct injection of Ach to brain causes stimulation followed by
depression.
Uses : Acetylcholine is not used ,
• Methacholine- PSVT.
• Bethanechol used in post operative urinary retention
gastroesophageal reflux, Pilocarine used as miotic in open angle
glaucoma.
Side effects: Defecation, sweating, fall in bp, bronchospasm.
26. ANTICHOLINESTERASES
• Anticholinesterase are agents which inhibit cholinesterase and rotect acetylcholine
from hydrolysis.
Classification
Reversible.
a)Carbamates
Physostigmine , neostigmine, pyridostigmine,
b) Acridine : Tacrine.
Irreversible:
Organophoshates:
Dyflos, ecothiophate, parathion, malathion.
Carbamates:
Carbaryl, Propoxur.
Chemistry: These are either esters of carbamic acid or derivatives of phosphoric acid.
27. Mechanism of action.
Cholinesterase enzyme contains two sites called as
aromatic anionic site and esteratic
site,cholinesterase enzyme is responsible for
hydrolysis of acetylcholine .
Anticholinesterases such as edrophonium and
tacrine attach to anionic site of cholinesterase
enzyme and inhibit it,
organophosphates attach only to esteratic site and
inhibit cholinesterase.
28. Pharmacological actions:
Ganglia:Ganglia is stimulated. High doses cause persistent
depolarization and blockade of transmission.
CVS: Muscarinic action reduces hypotension and bradycardia,
whereas ganglionic stimulation causes increase in heart
rate and bp.
Skeletal muscles: They cause twitching fibres and
fasiculations. High doses causes persistent depolarization of
end plates resulting in blockage of neuromuscular
transmission and causing weakness and paralysis.
Other effects: They cause stimulation of smooth muscles and
glands of gastrointestinal, respiratory, urinary tract and eye.
29. Uses
• Used as miotic,
• In glaucoma
• Myasthenia gravis
• In post operative paralytic ileus(0.5 mg-1 mg s.c neostigmine)
• Post operative decurarisation( 0.5 mg-2.0 g i.v neostigmine)
• In cobra bite(Neostigmine+atropine)
• In belladonna poisoning(Physostigmine-0.5-2 mg)
• Other drug overdosages( in tricyclic
antidepressant/phenothiazine/antihistaminic poisoning –
Physostigmine prevents the toxicity of above drugs)
• In alzheimers disease- Tacrine, rivastigmine, donepezil and
galantamine
31. Anticholinesterase poisoning(pesticide or
organophosphorous poisoning )
Anticholinesterases are easily available as agricultural and
household insecticides.
Occurs due to accidental use/intentional (suicidal)use of
anticholinesterases
Symptoms:
Irritation of eye, lacrymation, salivation, sweating, blurred
vision ,defeacation and urination
Fall in B.P, cardiac arrhythmias
Muscular fasiculations, weakness, respiratory paralysis
Excitement, ataxia, convulsions, coma and
Death
32. TREATMENT:
Termintaion of further exposure to poison.- fresh water
wash the skin, mucous membranes, perform gastric
lavage
Maintain patient airway.
Supportive measures- maintain blood pressure, control of
convulsions,
Specific antidotes:
Atropine, Cholinesterase reactivators such as pralidoxime.