ANS Adrenergic System (Medlive by DR Priyanka)

ANS
Dr. PRIYANKA SACHDEV , MD
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ANS –Cholinergic System ANS – Adrenergic System
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Dr. PRIYANKA SACHDEV

CNS
• Brain
• Spinal cord

PNS
Consists of nerves arising from brain and spinal cord

There are
• 12 pairs of cranial nerves

• 31 pairs of spinal nerves

TYPES OF NERVES
➢Afferent/ sensory nerves → carry signals from the
effector organs to CNS
➢Efferent / motor nerves → carry signals from the

CNS to the effector organs

Efferent nerves → carry signals from the CNS to the effector
organs
1. If carry signals from the CNS to skeletal muscle → Somatic

system (Voluntary)
2. If carry signals from the CNS to smooth muscle/ visceral

organs → Autonomic system (Involuntary) →Autos = self;
nomus = governing

• Somatic system carries nerve impulses from CNS to the
effector organs (skeletal muscle) by single effector
neurons (myelinated)
• ANS carries nerve impulses from CNS to the effector organs

by two types of effector neurons →
➢Preganglionic neuron (myelinated)
➢Postganglionic neuron (non myelinated)

Autonomic nervous system (ANS)
SYMPATHETIC PARASYMPATHETIC

Parasympathetic (Relaxed state) →
• Craniosacral (3 ,7, 9, 10)
• Ganglia → On or close to the organ supplied ie. away from spinal cord
• Preganglion Fibre → Long
• Postganglion fibre → Short
• Pre: post ganglionic ratio → 1: 1
Sympathetic (emergency , fight, fright) →

• Dorsolumber
• Ganglia → Close to spinal cord ie. away from the organs supplied
• Preganglion Fibre → Short
• Postganglion fibre → Long
• Pre: post ganglionic ratio → 1: 20 to 1: 100
Neurotransmitter (NT)
NT at somatic fibres →
• Acetylcholine (ACh) is the principal neurotransmitter (NT)

NT
Somatic ANS
Sympathetic Parasympathetic
Pregang. Postgang. Pregang. Postgang
Ach Nor adrenaline Ach Ach

Adrenaline
Dopamine
Ach
• Parasympathetic system → NT at effector organ is Ach →
So this system is known as CHOLINERGIC SYSTEM
• Sympathetic system → NT at effector organ is Adrenalin →

So this system is known as ADRENERGIC SYSTEM

ACTIONS
• Generally both Parasympathetic and Sympathetic nerve
fibers innervate an organ with usually opposite effects

4 chapters
• Cholinergic / Parasympathomimetics Drugs
• Anticholinergic / Parasympatholytics Drugs
• Adrinergic / Sympathomimetics Drugs
• Antiadrenergic / Sympatholytics Drugs

Cholinergic / Parasympethetic
system

Acetylcholine (ACh)
• In Cholinergic / Parasympathetic system →

Acetylcholine (ACh) is a major neurohumoral transmitter
at preganglionic as well as postganglionic fibres

Synthesis, storage, Release,
destruction of ACh
Synthesis and storage of ACh
Choline is taken up by cholinergic neurons by a specific
transport system (Na+: choline cotransporter) → Rate limiting
step
Acetyl Co-A donates acetyl group to choline, to form

acetylcholine with help of enzyme choline acetyl transferase in
axoplasm
Active transport of ACh into synaptic vesicles
Acetylcholine is then stored in vesicles

Release of ACh
With the arrival of nerve impulse
depolarization
influx of calcium into axoplasm
fusion of axonal and vesicular membrane
release of acetylcholine
Acts on M and N receptors

• Choline uptake is blocked by hemicholinium.
• Active transport of ACh into synaptic vesicles is inhibited by

vesamicol
• The release is blocked by botulinum and tetanus toxins and

promoted by latrotoxin, the toxin vendm of black widow spider

Destruction of ACh
Acetylcholine acts on the cholinergic M and N receptors
remains bound there for less than a millisecond
Hydrolyzed by cholinesterase enzyme (acetyl cholinesterase or

Butyrylcholinesterase)
About half of choline is recaptured by neurons and rest is carried

away in the circulation.
There's no reuptake of acetylcholine as occurs with other

transmiters
Cholinoreceptors
Two classes of receptors for ACh are recognized→
• Muscarinic (M) → G protein coupled receptor

• Nicotinic (N) → Ligand gated cation channel

Adrenergic Drugs
• Adrenergic drugs mimic the action produced by
sympathetic nerve stimulation hence also known as
sympathomimetics

BIOLOGICAL SYMPATHETIC
SUBSTANCES
• Nor adrenaline releases from postganglionic sympathetic
nerve fibers and adrenal medulla.
• Adrenaline releases from adrenal medulla.
• Dopamine releases from Basal ganglion

• NA acts as main neurotransmitter at postganglionic
sympathetic sites (except sweat glands, hair follicles
and some blood vessels)

SYNTHESIS , STORAGE AND RELEASE ,
Uptake and Metabolism of
catecholamines
SYNTHESIS

Phenylamine → Tyrosine (in liver)
L-tyrosine, an amino acid present in body fluids is taken up by adrenergic

neurons
In neurons, it is converted into DOPA (Dihydroxyphenylalanine) in presence of

tyrosine hydroxylase, which is a rate-limiting enzyme
DOPA is converted into dopamine in presence of DOPA decarboxylase
Dopamine is then converted to noradrenaline in presence of dopamine B

hydroxylase (inside vescicle)
In adrenal medulla and CNS noradrenaline is converted into adrenaline by

PNMT (phenyl ethanolamine N methyl transferase).
• Synthesis of NA occurs in all adrenergic neurons
• Synthesis of adrenaline occurs only in the adrenal

medullary cells

STORAGE AND RELEASE
Tyrosine is taken up by adrenergic nerve endings
Synthesis of dopamine
Transported to vehicles
Synthesis and storage of nor adrenaline occurs
NA is then stored as a complex with ATP (in a ratio of 4 : 1)

which is adsorbed on a protein chromogranin
Action potential generation
Influx of Ca++
Fusion of vesicles to the axonal membrane
Exocytosis
Uptake of catecholamines

1. Axonal uptake (uptake -1)
• It takes up NA at a higher rate than Adr.

• It is by an active amine pump NET which transports
NA by a Na+ coupled mechanism.
• This uptake is most important for terminating the
postjunctional action of NA
• It is blocked by cocaine.

2. Vesicular uptake
• It is by another amine pump vesicular monoamine

transporter (VMAT-2).
• Transports CA from the cytoplasm to the interior of the
storage vesicle.
• This transports monoamines by exchanging with H+.
• This uptake is important in maintaining the NA content
of the neuron.
• It is blocked by reserpine.
3. Extraneuronal uptake (uptake-2)
• Carried out by extraneuronal amine transporter (ENT

or OCT3) and other organic cation transposes OCT1
and OCT2.
• It takes up Adr at a higher rate than NA.
• It is not Na+ dependent
• It is inhibited by corticosterone

Metabolism of catecholamines
• Part of the NA leaking out from vesicles into cytoplasm as well as
that taken up by axonal transport is first attacked by MAO
• That NA which diffuses into circulation is first acted upon by

catechol-o-methyl transferase (COMT) in liver and other tissues.
• In both cases, the alternative enzyme can subsequently act to

produce vanillylmandelic acid (VMA).
• The major metabolite excreted in urine are VMA and 3-methoxy-4-

hydroxy phenylethylene glycol
• Metabolism does not play an important role in
terminating the action of neuronally released
(endogenous) CAs.
• It is axonal reuptake that is responsible for terminating

the action of endogenous CAs
• However, exogenously administered agents are primarily

metabolized by MAO and COMT
• Guanethidine is used for sympathectomy in
experimental animals

Compare

RECEPTORS
Cholinergic

Adrenergic

• Adrinergic drugs
• Antiadrinergic drugs

POLLS 1

D

C

Which of the following inhibits the rate
limiting step in synthesis of epinephrine -
• a) Guanithidine
• b) Bretylium
• c) Metyrosine
• d) Peserpine

C

Drug used for sympathectomy in
experimental animals is -
• a) Guanethidine
• b) Atropine
• c) Diazoxide
• d) Thebaine

A

Adrenergic Drugs

OVERVIEW
• Classification / Drugs
• MOA
• Actions
• Uses
• Containdications
• Side effects

CLASSIFICATION
• Some of them are α agonist
• Some of them are β agonist
• Some of them are nonselective (both) agonist

POLLS 2

A

D

A
• Dexmedetomidine is centrally active a2 agonist (selective a2A).

• It is used as preanaesthetic medication and for sedation in critically
ill/ventilated patients in ICU.

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

MOA

• Direct sympathomimetics They act directly as agonists on α and/or β
adrenoceptors
➢Adr, NA, isoprenaline (Iso), phenylephrine, methoxamine,
xylometazoline, salbutamol
• Indirect sympathomimetics They act on adrenergic neurone to

release NA, which then acts on the adrenoceptors
➢tyramine, amphetamine.
• Mixed action sympathomimetics They act directly as well as

indirectly
➢ephedrine, dopamine, mephentermine
OVERVIEW
• MOA
• Actions
• Uses
• Side effects

ACTIONS
Blood vessels and BP
• Vasoconstriction (α)
• Vasodilatation (β2)
• Vasoconstriction (α1 receptors) predominate in skin,

mucosal, renal and sphlanchnic blood vessels.
• Vasodilatation (β2 receptors) predominate in skeletal
muscles, liver and coronary blood vessels
BP = CO X PR
➢Systolic blood pressure is determined by cardiac output
➢Diastolic BP (DBP) is determined by blood vessel status;

hence vasoconstriction leads to increase in DBP,

CRUX
• α1 → VASOCONSTRICTION → Increases DBP
• β2 → VASODILATATION → Decreases DBP
• Β1 → CARDIAC STIMULATION→ Increases SBP

NA
1. Rise in systolic BP (cardiac stimulation due to β1
action)
2. Rise in diastolic (VC due to α1action)
• Rise in mean BP
• It does not cause vasodilatation (no β2 action), peripheral

resistance increases consistently due to α action
CRUX

Isoprenaline
1. Rise in systolic (β1—cardiac stimulation)
2. Fall in diastolic BP (β2— vasodilatation)
• The mean BP generally falls.

CRUX

CRUX

Adrenaline
• At high concentration of adrenaline → α1 response
predominates
• At low concentration of adrenaline → β2 response

predominates

CRUX

• Adr produces →
1. Marked increase in both systolic as well as diastolic BP (at high

concentration α1 response predominates and
vasoconstriction).
2. The BP returns to normal within a few minutes
3. A secondary fall in mean BP follows → The mechanism is—
rapid uptake and dissipation of Adr → concentration around the
receptor is reduced → low concentrations are not able to act on
α receptors but continue to act on β2 receptors.

• When an α blocker has been given, only fall in BP is
seen— vasomotor reversal of Dale.

DOPAMINE
• It is a dopamine
1. D1 and D2 agonist
2. α agonist
3. β1 agonist (not β2 agonist).

CRUX

Low dose
• The D receptors in renal and mesenteric blood vessels are
the most sensitive
• I.v. infusion of low dose (2-10 ug/kg/min) of dopamine

dilates these vessels

Moderate dose
• Moderately high doses (2-10 ug/kg/min) produce a
positive ionotropic effect (direct β1 action), but little
chronotropic effect on heart
• The advantage of this greater inotropic effect (increased

force of contraction) than chronotropic effect (increased
heart rate) of dopamine is that it produces smaller
increase in oxygen demand by the heart.

High dose
• Large doses (>10 ug/kg/min) produce vasoconstriction
(α1 action).
• At high doses, it is called inoconstrictor because it has

inotropic and vasoconstrictor effect.

Dopamine produces dose dependent action:
• i) At low dose (1-2 pg/kg/min) causes dilation of renal and mesentric

vessels -» often referred as renal dose.
• ii) At moderately high dose (2-10 pg/kg/min) produces a positive

ionotropic effect by stimulating px receptor on heart -» cardiac dose.
• iii) At high doses (> 10 pg/kg/min) produces vasoconstriction by

stimulating cy receptors -» vascular dose.

Use
• In normally employed doses, it raises cardiac output and
systolic BP with little effect on diastolic BP.
• It is used in cardiogenic or septic shock and severe CHF

wherein it increases BP and urine outflow.
• T1/2 of dopamine is 2 minutes

➢Low) dose of dopamine is antagonized by haloperidol
(dopamine antagonist)
➢Moderate dose is antagonized by β- blockers

(propranolol)
➢High dose by α-blockers (phentolamine)

Dobutamine
• Dobutamine is a relatively selective β1 agonist
• Though it acts on both α and β1 receptors, the only

prominent action of clinically employed doses is its β1
action
• i.e. an increase in force of cardiac contraction and

output, without a significant change in HR., BP and
Peripheral resistance
• Half life of dobutamine is 2 minutes
• Duration of action is less than 10 minutes
• onset of action after 1 -2 minutes.

DOBUTAMINE

USE
• Only prominent action is increase in force of cardiac
contraction and output (without significant change in
heart rate, peripheral resistance, and BP).
• It is used as an inotropic agent in pump failure

accompanying mycardial infarction, cardiac surgery, and
for short term management of severe congestive heart
failure.
Cardiogenic shock
• Drugs used in cardiogenic shock are -» Dobutamine,
Dopexamine or dopamine.
• “Dobutamine is preferred as it tends to vasodilate’

CRUX
Dopamine → D1 and D2 , α1 , β1 agonist

Dobutamine → selective β1 agonist

POLLS 3

Sympathomimetic drug which causes
decrease in heart rate -
• a) Adrenaline
• b) Isoprenaline
• c) Noradrenaline
• d) None

C

CRUX


D
• Norepinephrine causes rise in both systolic and diastolic BP.

• Ephedrine acts indirectly by releasing NA, so effect on BP will be the same as
NA.
• Adrenaline usually causes rise in systolic and fall in diastolic BP.
• Dopamine causes rise in systolic BP without an effect on diastolic BP.

C

CRUX


Dale’s vasomotor reversal –
• a) Stimulation of alpha-1 receptors

• b) Stimulation of alpha-2 receptors
• c) Stimulation of beta-1 receptors
• d) Stimulation of beta-2 receptors

D

Dale’s vasomotor reversal is due to -
• a) Alpha blocker
• b) Beta blocker
• c) ACH inhibitor
• d) All of the above

A

Dales vasomotor reversal phenomenon occurs
with-
• a) Dopamine
• b) Adrenaline
• c) Nor Adrenaline
• d) All of the above

B

Most potent cardiac stimulant of the following
is -
• a) Adrenaline
• b) Noradrenaline
• c) Ephedrine
• d) Salbutamol

A

D

A

D

CRUX


C

CRUX


A

A

CRUX


A

A

Heart (β1)
Stimulates the heart to
• Increase the rate (Positive chronotropic),
• Increase force of contraction (Positive inotropic),
• Increase conduction (Positive dromotropic)
• Adrenaline also increases the conduction velocity of the

heart so there is an increase risk of arrhythmia.

Respiration
• Adr and isoprenaline, but not NA are potent
bronchodilators (β2)
• Adr given by aerosol additionally decongests bronchial

mucosa (α)

Eye
• Mydriasis (α1) occurs due to contraction of Dilator
pupillae) of iris

A. Mydriasis (dilatation of pupil)
• i) Sympathomimetic drugs (at agonists): By contraction of
dilator pupillae muscles
• ii) Parasympatholytic / Antimuscarinic drugs: By blocking the
action of sphincter pupillae muscles
B. Miosis (constriction of pupil)

• i) Parasympathomimetic (muscarinic) drgus: By stimulating the
contraction of sphincter pupillae muscles
• ii) Sympatholytic drugs (a1 antagonists): By blocking the action
of dilator pupillae muscles

A. Mydriasis (dilatation of pupil)
• i) Sympathomimetic drugs (at agonists): By contraction of dilator
pupillae muscles
• ii) Parasympatholytic / Antimuscarinic drugs: By blocking the
action of sphincter pupillae muscles
B. Miosis (constriction of pupil)

• i) Parasympathomimetic (muscarinic) drgus: By stimulating the
contraction of sphincter pupillae muscles
• ii) Sympatholytic drugs (a1 antagonists): By blocking the action
of dilator pupillae muscles

4 chapters
• Cholinergic / Parasympathomimetics→ miosis
• Anticholinergic / Parasympatholytics → mydriasis
• Adrinergic / Sympathomimetics→mydriasis
• Antiadrenergic / Sympatholytics → miosis

• Intraocular tension tends to fall → useful in glaucoma

GIT
1. Smooth muscle Relaxation ( both α and β receptors)
2. Sphincters are constricted ( α receptors)
• peristalsis is reduced → Constipition

• but the effects are brief and of no clinical import.

Bladder
• Detrusor is relaxed (β) and sphinctor is constricted
(α): both actions tend to hinder micturition → urinary
retention.

Uterus
• Adr can both contract (α1 ) and relax uterine muscle
(β2)
• The overall effect varies with species, hormonal and
gestational status.
• Human uterus is relaxed by Adr at term of pregnancy,

but at other times, its concentrations are enhanced.

Splenic capsule
• Contracts (α1)
• More RBCs are poured in circulation.
• This action is not evident in man.

Insulin and glucagon secretion
• Reduction of insulin (α2)

• Augmentation of glucagon (β2) secretion.

Metabolic
• Liver—glycogenolysis (α and β2) → hyperglycaemia
• Muscle—glycogenolysis (β2) → hyperlactacidaemia
• Fat—lipolysis (β1 + β2 + β3) → increased blood FFA,
• Calorigenesis
• These are due to direct action on liver, muscle and
adipose tissue cells.

Kidney
• Increased renin release (β1 receptors)

Male sex organ
• Ejaculation (α1)

CNS
• Restlessness, apprehension and tremor (β2) may
occur

POLLS 4

A

A

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

THERAPEUTIC USES
1. Pressor Agents (α agonist)

(i) Hypotensive states
• Shock, spinal anaesthesia, hypotensive drugs
• One of the pressor agents can be used along with volume

replacement for neurogenic and haemorrhagic shock

Anaphylactic shock
• Adr 0.5 mg injected promptly i.m. is the drug of
choice in anaphylactic shock
• It raises BP, and also counteracts bronchospasm/
laryngeal edema that may accompany.
• Because of the rapidity and profile of action Adr is the
only life saving measure

First adrenaline should be given im to raise the blood
pressure and to dilate the bronchi.
If the treatment is delayed and shock has developed,

adrenaline should be given i.v. by slow injection.

• Both subcutaneous and intramuscular routes are
recommended for adrenaline use in anaphylactic shock.
• However, intramuscular route of administration is

superior and therefore is the route of choice for the
treatment of anaphylactic shock. The lateral aspect of
thigh is the site of choice.
• Subcutaneous route is second choice.

(ii) Along with local anaesthetics
• Adr 1 in 200,000 to 1 in 100,000 for infiltration, nerve
block and spinal anaesthesia.
1. Duration of anaesthesia is prolonged

2. systemic toxicity of local anaesthetic is reduced.
3. Local bleeding is minimised

(iii) Control of local bleeding
• From skin and mucous membranes, e.g. epistaxis :
compresses of Adr 1 in 10,000,
phenylephrine/ephedrine 1% soaked in cotton can
control arteriolar and capillary bleeding.

(iv) Nasal decongestant
• In colds, rhinitis, sinusitis, blocked nose → one of the α-
agonists is used as nasal drops.
• Shrinkage of mucosa provides relief

1. Regular use of these agents for long periods should be
avoided because mucosal ciliary function is impaired
2. Atrophic rhinitis and anosmia can occur due to
persistent vasoconstriction.
3. They can be absorbed from the nose and produce
systemic effects, mainly CNS depression and rise in BP

2. Cardiac stimulants (β1
agonist)

(i) Cardiac arrest
• Adr may be used to stimulate the heart
• Epinephrine (1:1000 concentration) is the drug of

choice in CPR.

(ii) Partial or complete A-V block
• Isoprenaline may be used as temporary measure to
maintain sufficient ventricular rate.

(iii) Congestive heart failure
(CHF)
• Adrenergic inotropic drugs are not useful in the routine
treatment of CHF.
• However, controlled short term i.v. infusion of DA /

dobutamine can tide over acute cardiac
decompensation during myocardial infarction, cardiac
surgery and in resistant CHF.

3. Bronchodilators (β2 agonist)

• Bronchial asthma and COPD→ Adrenergic drugs,
especially β2 stimulants are the primary drugs for relief
of reversible airway obstruction

4. CNS

• (i) Attention deficit hyperkinetic disorder (ADHD):
• (ii) Narcolepsy
• (iii) Epilepsy
• (iv) Parkinsonism
• (v) Obesity→ It decreases apetite center (anorectic
drugs)

5. Uterine relaxant (β2 agonist)
• Isoxsuprine and Ritodrine has been used in
threatened abortion and dysmenorrhoea

6. EYE (α agonist)
• Mydriatic (α1 agonist)→Phenylephrine is used to
facilitate fundus examination
• Glaucoma (α2 agonist)→ Apraclonidine,

brimonidine→It tends to reduce intraocular tension

7. Urinary bladder
• Nocturnal enuresis in children and urinary
incontinence→ Amphetamine affords benefit both by
its central action as well as by increasing tone of vesical
sphincter.

8. Allergic disorders
• Adr is a physiological antagonist of histamine which is an
important mediator of many acute hypersensitivity
reactions.
• It affords quick relief in urticaria, angioedema;
• It is life saving in laryngeal edema and anaphylaxis.

REMEMBER

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

Adverse effects
1. Marked rise in BP leading to cerebral haemorrhage
2. Ventricular tachycardia/fibrillation, angina,

myocardial infarction

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

Contraindications
1. Hypertensive
2. Hyperthyroid
3. Angina patients

SUMMERY

POLLS 5

A
• First adrenaline should be given im to raise the blood pressure and to

dilate the bronchi.
• If the treatment is delayed and shock has developed, adrenaline should
be given i.v. by slow injection.

D
• Both subcutaneous and intramuscular routes are recommended for
adrenaline use in anaphylactic shock.
• However, intramuscular route of administration is superior and

therefore is the route of choice for the treatment of anaphylactic
shock. The lateral aspect of thigh is the site of choice.
• Subcutaneous route is second choice.

A
• Drugs used in cardiogenic shock are -» Dobutamine, Dopexamine or

dopamine.
• “Dobutamine is preferred as it tends to vasodilate’
•
• Dobutamine is not given in options, so best answer is dopamine.

D
• Epinephrine (1:1000 concentration) is the drug of choice in CPR.

C
• Prazosin is an a-1 blocker (not a-2 agonist).

A

Antiadrenergic Drugs
(Adrenergic Receptor
Antagonists)

• These are drugs which antagonize (block) the
receptor action of adrenaline
• They are competitive antagonists at α or β or both α

and β adrenergic receptors

α ADRENERGIC BLOCKING DRUGS B ADRENERGIC BLOCKING DRUGS

α ADRENERGIC BLOCKING
DRUGS

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

CLASSIFICATION

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

MOA
• These drugs inhibit adrenergic responses mediated
through the α adrenergic receptors without affecting
those mediated through β receptors

POLLS

A

C

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

ACTIONS OF α BLOCKERS

1. Blood vessels and BP
Blockade of vasoconstrictor α1 (also α2) receptors
Vasodilatation
fall in BP → hypotension
dizziness and syncope

• Adr produces →
1. marked increase in both systolic as well as diastolic BP (at
high concentration α response predominates and
vasoconstriction).
2. The BP returns to normal within a few minutes
3. a secondary fall in mean BP follows → The mechanism is—
rapid uptake and dissipation of Adr → concentration around
the receptor is reduced → low concentrations are not able to
act on α receptors but continue to act on β2 receptors.

• The α blockers abolish the pressor action of Adr (injected i.v.
in animals),
• So if we give adrenaline after α blockers then adrenaline

produces only fall in BP due to β2 mediated vasodilatation.
• This was first demonstrated by Sir HH Dale (1913) so called

vasomotor reversal of Dale.

• Nasal stuffiness result from blockade of α receptors
in nasal blood vessels

2. Heart
• Reflex tachycardia occurs due to fall in mean BP

3. Eye
• Miosis result from blockade of α receptors in Dilator
pupillae muscles of iris

4. Intestine
• Intestinal contraction is increased due to partial
inhibition of relaxant sympathetic influences→ loose
motion may occur.

5. Bladder
• Bladder sphincter and prostate is relaxed by blockade
of α1 receptors (mostly of the α1A subtype) → urine
flow in patients with benign hypertrophy of prostate
(BHP) is improved

6. Male sex organ
• α receptors causes ejaculation
• α blockers can inhibit ejaculation; this may manifest

as impotence

7.Na+and fluid retention
Due to hypotension, renal blood flow is reduced
Activation of renin angiotensin aldosterone system
Na+ & water retention

No effect
• The α blockers have no effect on→
1. cardiac stimulation,
2. bronchodilatation,
3. metabolic changes
• Because these are mediated predominantly through β

receptors.
OVERVIEW
• MOA
• Actions
• Uses
• Side effects

USES OF α BLOCKERS

1. Hypertension
• Only selective for α1 receptors (prazosin-like) are used→
they decreases BP by vasodilatation
• α blockers other than those selective for α1 are not used

because reflex tachycardia, postural
hypotension,impotence, nasal blockage and other side
effects produced

2. Pheochromocytoma
• Pheochromocytoma is tumour of adrenal medullary cells

• It is a catecholamine- secreting tumor of chromatin tissue.
• Excess CAs are secreted which can cause intermittent or
persistent hypertension.
• Estimation of urinary CA metabolites (VMA,
normetanephrine) is diagnostic
• Surgery is the definitive therapy

Inoperable and malignant
pheochromocytoma
• Phenoxybenzamine can be used as definitive therapy for
inoperable and malignant pheochromocytoma.
• Prazosin is an alternative

• In operable cases → Before and during surgery, α and
β blockers are given to block α and β receptors to avoid effects
of massive sudden release of catecholamines due to handling
of tumour
• Irreversible α blocker is preferred because a huge release of

catecholamine may overcome the effect of reversible blocker.
• If an immediate effect is necessary then phentolamine is

preferred

REMEMBER
➢Phenoxybenzamine is the DOC for inoperable
tumour or to control BP before surgery
➢Phentolamine is the DOC for hypertensive crisis or

for intraoperative BP control

3. Secondary shock
• Shock due to blood or fluid loss is accompanied by reflex
vasoconstriction.
• α blocker (phenoxybenzamine i.v.) can help by

counteracting vasoconstriction by vasodilatation
• Volume replacement also given

4. Peripheral vascular diseases
• when vasoconstriction is a prominent feature
(Raynaud’s phenomenon, acrocyanosis), α1 blocker (
prazosin or phenoxybenzam) provide good symptomatic
relief by vasodilatation

5. Congestive heart failure (CHF)
• The vasodilator action of prazosin can afford symptomatic

relief in selected patients of CHF by decreasing preload

6. Prinzmetal's angina
• It is the outcome of coronary vasospasm;
• therefore a blocker helps by relieving it owing to
vasodilatation

7. Male impotency due to erectile
dysfunction
Intracavernous injection of phentolamine produces erection
(by causing vasodilatation of penile blood vessels ) to improve
erectile dysfunction.
• But there is risk of priapism

• need for a specialist to give the injection
• Repeated injections can cause penile fibrosis.
hence orally effective drug like sildenafil is preferred.

8. Hypertension due to clonidine
withdrawl, cheese reaction
• Phentolamine is used for control of hypertension due to

clonidine withdrawl, cheese reaction (Vasodilatation)

9. Benign hypertrophy of prostate
(BHP)
• The urinary obstruction caused by BHP has a static
component due to increased size of prostate and a
dynamic component due to increased tone of bladder
sphincter/prostate smooth muscle.

• Two classes of drugs are available:
1.α1 adrenergic blockers (prazosin like): Relaxes
prostatic/bladder sphincter muscles.
2.5-α reductase inhibitor (finasteride) (testosterone

synthesis inhibitor): arrest growth/reduce size of
prostate

• Temsulosin and silodosin, ( α1A selective blockers) are
preferred agents as they do not cause postural
hypotension
• Terazosin and doxazosin promote apoptosis in

prostate → prostate size.

OVERVIEW
• MOA
• Actions
• Uses
• Side effects

Side effects of α blockers
1. Postural hypotension (most important) → Which is

usually seen with first few doses (first dose effect)
2. Nasal blockade
3. Palpitation
4. Loose motions
5. Inhibition of ejaculation and impotence.
6. Fluid retention
OVERVIEW
• MOA
• Actions
• Uses
• Side effects

SUMMERY

POLLS

A

A

B

B

α ADRENERGIC BLOCKING DRUGS B ADRENERGIC BLOCKING DRUGS

β ADRENERGIC BLOCKING
DRUGS

SUMMERY OF
ANS

Cholinergic / Anticholinesterase
drugs

Anticholinergic / Antimuscarinic
drugs Drugs

α and β agonist

DRUGS

DRUGS

THANK YOU

REVISION

α and β agonist

DRUGS

DRUGS

THANK YOU

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Friday)→PATHOLOGY
• Every TTS (Tuesday , Thursday , Saturday) →

PHARMACOLOGY

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ANS
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ANS –Cholinergic System ANS – Adrenergic System
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ANS Adrenergic System (Medlive by DR Priyanka)

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ANS

Dr. PRIYANKA SACHDEV , MD

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Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Consists of nerves arising from brain and spinal cord

Dr. PRIYANKA SACHDEV

• 12 pairs of cranial nerves

Dr. PRIYANKA SACHDEV

➢Efferent / motor nerves → carry signals from the

Dr. PRIYANKA SACHDEV

1. If carry signals from the CNS to skeletal muscle → Somatic

2. If carry signals from the CNS to smooth muscle/ visceral

Dr. PRIYANKA SACHDEV

• ANS carries nerve impulses from CNS to the effector organs

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Sympathetic (emergency , fight, fright) →

Dr. PRIYANKA SACHDEV

Pregang. Postgang. Pregang. Postgang

Ach Nor adrenaline Ach Ach

• Sympathetic system → NT at effector organ is Adrenalin →

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

• In Cholinergic / Parasympathetic system →

Dr. PRIYANKA SACHDEV

Acetyl Co-A donates acetyl group to choline, to form

Active transport of ACh into synaptic vesicles

Acetylcholine is then stored in vesicles

influx of calcium into axoplasm

fusion of axonal and vesicular membrane

Acts on M and N receptors

• Active transport of ACh into synaptic vesicles is inhibited by

• The release is blocked by botulinum and tetanus toxins and

Dr. PRIYANKA SACHDEV

remains bound there for less than a millisecond

Hydrolyzed by cholinesterase enzyme (acetyl cholinesterase or

About half of choline is recaptured by neurons and rest is carried

There's no reuptake of acetylcholine as occurs with other

Two classes of receptors for ACh are recognized→

• Muscarinic (M) → G protein coupled receptor

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

Dr. PRIYANKA SACHDEV

L-tyrosine, an amino acid present in body fluids is taken up by adrenergic

In neurons, it is converted into DOPA (Dihydroxyphenylalanine) in presence of

DOPA is converted into dopamine in presence of DOPA decarboxylase

Dopamine is then converted to noradrenaline in presence of dopamine B

In adrenal medulla and CNS noradrenaline is converted into adrenaline by

• Synthesis of adrenaline occurs only in the adrenal

Dr. PRIYANKA SACHDEV

Synthesis and storage of nor adrenaline occurs

NA is then stored as a complex with ATP (in a ratio of 4 : 1)

Fusion of vesicles to the axonal membrane

Dr. PRIYANKA SACHDEV