OVERVIEW OF ANS SYMPATHETIC SYSTEM PREGANGLIONIC AND POST GANGLIONIC FIBERS DISTRIBUTION OF SYMPATHETIC FIBERS SYNTHESIS OF CATECHOLAMINES AND THERE INHIBITION AT VARIOUS LEVELS RECEPTORS OF SYMPATHETIC SYSTEM SYMPATHOMIMETIC DRUGS *DIRECTLY AND INDIRECTLY ACTING DRUGS* SYMPATHOLYTIC DRUGS USES OF THESE DRUGS SUMMARY ADDITIONAL INFO :ALPHA 2 RECEPTORS ARE MAJORLY PRESENT IN CNS AND DRUG USED IS CLONIDINE

1. DR. SACHIN OJHA
DEPARTMENT OF ANAESTHESIOLOGY
T.S.M.M.C.H
MENTOR- DR NEHA SHARMA

2. DOPAMINE  IN KIDNEYS
ADRENALINE  IN ADRENAL MEDULLA
ACETYL CHOLINE  IN SWEAT GLANDS AND PILO
ERECTOR MS.
OVERVIEW

3. PARASYMPATHETIC SYMPATHETIC
HEART
BRONCHUS BRONCHOCONSTRICTION BRONCHODILATATION
GIT DIARRHEA ( INC SECRETION
AND MOTILITY)
CONSTIPATION (DEC
SECRETION AND MOTILITY)
BLADDER INCREASE OUTFLOW
(CONTRACTING DETRUSOR
AND RELAXING TRIGOME)
DECREASE OUTFLOW
(RELAXING DETRUSOR
AND CONTRACTING
TRIGOME)
GLANDS INCREASE SECRETIONS DECREASE SECRETIONS
PUPIL MIOSIS MYDRIASIS

4. Definition
• Sympathetic nerves originates in the spinal
cord along with spinal nerves between cord
segments T1 and L3 [Thoraco-Lumbar region].
• Each sympathetic pathway from the cord to
the stimulated tissue is composed of two
neurons , a Preganglionic neuron and a
postganglionic neuron .
• The sympathetic nervous system’s primary
process is to stimulate Fight fright and flight
response.

5. Preganglionic
o Preganglionic sympathetic nerve fibres-
• these are short , myelinated and type B fibres.
• Originates in thoracolumbar division of the
spinal cord specifically at T1 to L2~L3 , and
travels to a ganglion .
• Then they synapse with a postganglionic
neurons .
• These fibres are cholinergic and use
acetylcholine as their neurotransmitter.

6. Postganglionic
o Postganglionic sympathetic fibres –
• Arises from sympathetic ganglia
• These are long , non myelinated and type C
fibres
• These fibres are adrenergic and use
norepinephrine as a neurotransmitter.

7. Distribution of Sympathetic neurons
Segmental level
• T1,T2
• T3 ,T4
• T5 to T9
• T10 to L2
• T6 to T12
• L1,L2
• T1 to T12
Area of distribution
• Head & Neck
• Thoracic viscera
• Upper limb
• Lower limb
• Upper abdominal viscera
• Lower abdominal viscera
• Thoracic & abdominal
vessels

8. Metyrosine is a competetive inhibitor of tyrosine hence lesser tyrosine less norad production
RESERPINE MOA IS through inhibition of the ATP/mg2+ pump responsible for the sequestering of
neurotransmitters into storage vesicles located in the presynaptic neuron.
Guanethidine is a sympatholytic drug that acts by displacing norepinephrine from postganglionic
sympathetic nerve endings. The drug depletes tissue stores of norepinephrine, decreases reuptake of
norepinephrine by the nerve terminals, and lowers sympathetic tone.
COCAINE inhibits NET resulting in increased NA hence increased sympathetic activity.

9. RECEPTORS
Also present on urinary bladder mirabegron (in over active bladder)

10. Effects of sympathetic stimulation
(DIALATOR PUPILLAE MS)

12. SYMPATHOMIMETICS
{DIRECTLY ACTING}
• Catecholamines - Name is based on their chemical
structure (hydroxyl groups at the 3 and 4 position of a
benzene ring):
– High potency - activate both alpha and beta receptors
– Rapid inactivation - Destroyed by COMT (Catechol O-
methyltransferase) and by MAO (Monoamine oxidase)
which are present in the gut wall. hence Catecholamines
are not effective when given orally
– Poor CNS penetration - They are polar but they still may
cause some CNS effects

13. • Non-catecholamines -
– Not destroyed by COMT and MAO deactivation is
limited, so they have longer half lives
– Better CNS penetration due to increased lipid
solubility

14. CATECHOLAMINES
ENDOGENOUS
• ADRENALINE
• NOR ADRENALINE
• DOPAMINE
EXOGENOUS
• DOBUTAMINE
• ISOPRENALINE
• FENOLDOPAM

15. DOPAMINE
SHOCK
Dopaminealpha-1 vasoconstriction↑BP
~Also in shock BP↓↓filtration and pressure leading to renal
failure.
~So in shock with oligouria DOC is DOPAMINE as it also stimulates
D1 receptor which causing VD resulting in ↑filtration.
0.2-1mg/min regulated by monitoring bp and urine output.
CHF
Stimulates beta-1 receptors  ↑ heart reate

16. DOBUTAMINE
• Stimulates beta-1 receptors
– CHF 5-20mcg/kg/min
– DOBUTAMINE STRESS TESTING IN ANGINA
• 10mcg/kg 3 mins203040
FENOLDOPAM
• Stimulates D-1 receptors
 Used in hypertensive emergencies and severe
hypertention 0.1-1.6 mcg/kg/min

17. CNS
↑DBP
↓DBP
↑ SYMPATHETIC
↑HEART RATE
↑PARASYMPATHETIC
↓HEART RATE
BARO -RECEPTORS

18. Adrenaline , Nor adrenaline ,
Isoprenaline

19. NOR ADRENALINE
• Stimulates alpha-1 , alpha-2 ,beta-1 receptors
– Alpha1 shock , hypertension
– Beta 1  ↑HR CHF
– 2-4mcg/min
ISOPRENALINE
• Stimulates BETA-1 and BETA-2 receptors
 Beta 1  ↑H.R. CHF
 Beta 2  Bronchodilatation ASTHMA
 20mg sublingual,1-2mg IM, 5-10mcg/min IV

20. ADRENALINE
1. Cardiac arrest C-A-B  adr 1:10000 (0.2-0.5mg)
– IV >intraosseus>endotracheal
2. ANAPHYLACTIC SHOCK
– ALPHA-1 TO INCREASE BP
– BETA 2 FOR BRONCHODILATATION
– Route im/sc 0.5ml 1:1000 solution(1gm adr in 1000ml
of solution) repeat every 10 mins
– If im fails iv adr 1:10000 solution to be given
3. ADRENALINE WITH LOCAL ANAESTHESIA
– ADR  VC Systemic flow of LA obstructed 
toxicity and shock chances ↓

21. Non catecholamines
• Alpha1 agonists
– Phenylephrinemydriasis fundoscopy
– Methoxamine,mephentermine ↑BP (in hypotention)
– Xylometazoline,oxymetazoline,naphazoline cause
vasoconstrictiondegongestant. Overuse causes atrophic rhinitis/
rhinitis medicamentosa.
• Alpha 2 agonists
– Clonidine low dose present presynaptic↓BP
– Also used to overcome withdrawl symptoms of drugs like
morphine
• Beta 2 agonists
– Salbutamol,terbutallineinhalational
routebronchodilatation bronchial asthma
– Ritodrine,isoxsuprine relaxes uterustocolytic(preterm labour)

22. SYMPATHOLYTICS:
Drugs that reduce or inhibit some or all of the actions of the
sympathetic nervous system.

24. α blocker
• α1+α2 blocker
• Selective and non selective α blockers are
used for mild to moderate hypertention

25. Selective α blocker
• α1 blocker
– vasodilation of BV (ind HTN)
– increase urine outflow (ind BPH)
– So pt with HTN+BPH can be administered with drugs
such as
• PRAZOSIN (0.5-1mg upto 4mg BD or TDS)
• TERAZOSIN
• DOXAZOSIN(1mg OD)
• ALFUZOSIN(2.5mg bd-qid or 10mg OD in er)
• These drugs may cause postural hypotension
hence given at bed time.

26. • On further research it was found out that α1
receptors are of two type α1a (majorly on
prostatic urethra) and α1b (on blood vessels)
• So for pt with BPH without HTN only α1a
blocker is given
– TAMSULOSIN (0.2-0.4mg)
– SILODOSIN(4-8mg)

28. ß blockers

29. Properties and drugs
• Cardioselective ß1 blocker
• Intrinsic sympathomimetic activity/partial
agonist
• Membrane stabilising property/Na+ channel
#/local anaesthetic
• Non lipid soluble/water soluble

30. 1. ß1# or cardioselective or 2nd gen
Safe in asthma ,PVD , DM

31. 2. Intrinsic sympathomimetic activity/partial
agonist
•Celiprolol
•Pindolol
•Alprenolol
•Acebutolol
3. Membrane stabilising property/ Na
channel blocker
Indicated in arrythmias
Not indicated in glaucoma as these drugs masks the corneal reflex
•Propanolol
•Metoprolol
•Labetalol
•Acebutolol
•Pindolol

32. 4. Water soluble
• Contraindicated in renal failure.
– ATENOLOL
– NADOLOL (LONGEST ACTING)
– SOTALOL

33. 3rd generation
• Posses properties of ß blocker and
vasodialation (α #)
– Labetalol
• Dose : 50mg BD, increase to 100-200mg TDS oral.
• In hypertensives emergencies 20-40mg iv every 10 mins
till desired effect is seen
– Carvedilol
• CHF: start with 3.125 mg bd for 2 weeks if well
tolerated gradually increase max upto 25mg BD
• Hypertension/angina: 6.25mg BD initially, titrate to max
25mg BD.

34. Uses of ß blocker