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
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.
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
15. DOPAMINE
SHOCK
Dopaminealpha-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 mins203040
FENOLDOPAM
• Stimulates D-1 receptors
Used in hypertensive emergencies and severe
hypertention 0.1-1.6 mcg/kg/min
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
– Phenylephrinemydriasis fundoscopy
– Methoxamine,mephentermine ↑BP (in hypotention)
– Xylometazoline,oxymetazoline,naphazoline cause
vasoconstrictiondegongestant. 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,terbutallineinhalational
routebronchodilatation bronchial asthma
– Ritodrine,isoxsuprine relaxes uterustocolytic(preterm labour)
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)
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.