ADRENERGIC SYSTEM

Dr. DEVENDRA PARAZ

Autonomic Nervous System
a. Parasympathetic Nervous System
Participates in tissue building reaction.

b. Sympathetic Nervous System.

Prepares the body for fight or flight.
FIGHT-FRIGHT-FLIGHT
Sympathetic/ adrenergic system
 Adrenergic Drugs or
Sympathomimetic Drugs
 Drugs that mimic the response

obtained as a result of stimulation

of the sympathetic or adrenergic nerves.

 Adrenergic Drugs
1. Catecholamines compounds containing
a. Catechol nucleus i.e. a benzene ring with
two adjacent 0H groups &
b. An amine containing side chain.

2. Non-catecholamines
Lacks the hydroxyl group.
 Catecholamines
1. Noradrenaline (NA): It act as a transmitter at
postganglionic sympathetic sites.

2. Adrenaline (Adr): Secreted by adrenal

medulla.

3. Dopamine (DA): It is a major transmitter in

basal ganglia, limbic system.
Noradrenaline (Norepinephrine)
Nor in noradrenaline means
N nitrogen
O ohne (without)
R radical ( methyl group)
Synthesis of catecholamines
Phenylalanine ( dietary amino acid)
liver hydroxylase
Tyrosine
adrenergic tyrosine hydroxylase
neuronal DOPA
cytoplasm DOPA decarboxylase
Dopamine
Inside β hydroxylase
vesicles Noradrenaline
adrenal N methyl transferase
medullary cells Adrenaline
 Synthesis
1. Noradrenaline or Norepinephrine
Adrenergic neurons

2. Adrenaline
Adrenal medulla
Termination of action
1. Neuronal uptake
a. Uptake 1 across the neuronal membrane into
the cytoplasm.
b. Granular uptake from the cytoplasm into the
storage vesicles

2. Uptake 2: Diffusion from the synaptic cleft to

extraneuronal tissues.

3. Biotransformation by MAO & COMT.

Adrenergic Receptors
Raymond Ahlquist 1948
α β

α1 α2 β1 B2 B3

α1A α1B α1D α2A α2B α2C

Adrenergic Receptors
1. α receptor stimulation is mainly responsible
for the excitatory effects of catecholamines
exception is in GIT.

2. β receptor stimulation is mainly responsible

for the inhibitory effects of catecholamines
exception is in Heart.
Tissue effects α1 β2

1.Smooth muscle

a. Blood vessels Constricts Dilates

b. Bronchi Dilates

c. GI Tract Relaxes Relaxes

d.GI spincters Contracts

e. Uterus Relaxes

f. Bladder detrusor Relaxes

g. Bladder spincter contracts

Tissue effects α1 β2

2. Iris (radial muscle) contracts

3. Skeletal muscle Tremors

4. Liver Glycogenolysis

5. Mast cells Inhibits histamine

release
Location Prejunctional on nerve ending
Inhibitor of transmitter release.

Brain decreases the central sympathetic

outflow.

α2 receptor
β1 Receptor
Postsynaptically

1. Heart Positive inotropic

Positive chronotropic
Positive dromotropic

2. Kidney promote renin release.

β2 receptor
Postsynaptically

1. Bronchi bronchodilatation.

2. Blood vessels supplying skeletal muscle &

coronary arteries vasodilatation.

3. Uterus uterine relaxation.

4. GIT relaxation
β3
Adipocytes

Activation promotes lipolysis &

thermogenesis.
Adrenergic drugs
1. Direct sympathomimetics
Act directly as agonists on α & or β receptors.
Adrenaline, noradrenaline & isoprenaline.
2. Indirect sympathomimetics
Act on adrenergic neurons to release NA
which then acts on the receptors.
Tyramine
3. Mixed acting sympathomimetics
Acts directly awa indirectly.
Ephedrine
Classification of adrenergic drugs
Pharmacological Actions
1. Adrenaline: α1+α2+ β1+β2+ β3 agonist

2. Noradrenaline: α1+α2+β1+β3 no β2
action

3. Isoprenaline: β1= β2, β3 no α action

Pharmacological actions
1. Heart increases force of contraction
increase heart rate
increases conduction.

Noradrenaline: When BP rises markedly reflex

bradycardia occurs due to stimulation of vagus.

Adrenaline: BP rises moderately &

is acompanied by tachycardia.
Blood vessels & Blood Pressure
Adrenaline& NA constricts the blood vs of the
skin & mucus membrane.

Adrenalinedilates the blood vessels of skeletal

muscles β2 & decreases the PVR.

Adrenaline increases systolic BP by its Cardiac action.

Adrenaline decreases diastolic BP by its Peripheral

action.

Not suitable in hypovolemic shock.

Blood vessels & Blood Pressure
Adrenaline: Rise in systolic BP foll. By a fall.

Biphasic response

Rise in sys. BP: Stimulation of α1 receptors.

Fall in sys. BP: Stimulation of β2 receptors.

α receptor action is dominant & short lasting.

β2 receptor action is persistent & long lasting.

large dose (4mcg/kg)
Rise in BP followed by a fall.

Rise due to
vasoconstrictor α receptors.

Fall due to vasodilator β2

receptors

Biphasic response with Adrenaline

 If α blocker (Tolazoline) is
given– only fall in BP is seen
(unmasking of beta action by
the α blocker).

Not seen with NA.

Dale’s Vasomotor reversal.

Dale’s vasomotor reversal
Sir Henry Dale

Biphasic response is converted to a

depressor
response by prior administration of alpha
receptor blocker.

Due to unopposed action of adrenaline on

β2 receptors.
 RS

a. Bronchi Bronchodilatation (β2).

b. Inhibits the release of mediators from the

mast cells (β2).

c. Decongestion: Constriction of blood vessels

of mm of URT (α1)
Gastrointestinal tract
Adrenaline & NA

Relax the smooth muscle of the gut.

Reduce its motility.

Spincters are constricted.

 Urinary Bladder
Detrussor is relaxed (β2).

Trigone & spincter is constricted (α1).

Both actions hinder micturition.

Ductus deferens, seminal vesicles & prostate

(α1) contraction ejaculation

 Uterus
Non pregnant uterus contracts.

Last month of pregnancy relaxes.

 Eye
Adrenaline causes mydriasis

due to contraction of the radial muscle

of the iris α1.

Reduces intraocular pressure.

 Metabolic effects
Adrenaline increases the blood sugar level.

a. By enhancing hepatic glycogenolysis (β2).

b. Reducing insulin secretion .

c. Decreases uptake of glucose by peripheral

tissues.
 Pharmacokinetics
Catecholamines are not given orally.

 Rapidly inactivated in the gut & liver.

Adrenaline
& NA are metabolised
by COMT & MAO.
Adverse Effects
1. Transient restlessness

2. Palpitation

3. Anxiety

4. Tremor

5. Pallor

6. Marked rise in BP IV inj.

Contraindication
1. Hypertensive.

2. Hyperthyroid.

3. Angina.
Drug Interactions
β blockers - marked rise in BP

d/t unopposed α action.

Indications of Adrenaline
1. Anaphylactic shock DOC

Acute Hypersensitivity reaction

d/t massive release of mediators
like histamine & bradykinin.
Anaphylactic shock
a. Laryngeal edema.
b. Severe bronchoconstriction.
c. Peripheral vasodilatation.
d. Hypotension
e. Cardiovascular collapse.

Death occurs due to

a. Airway obstruction
b. CV collapse.
 Anaphylactic shock
1. Natural antagonist of histamine.

2. α1 stimulation causes vasoconstriction

decreases laryngeal edema.

3. β2 inhibits release of mediators from mast

cells & basophils.

4. β2 bronchodilatation.

5. β1 action on heart increasing HR &

force of contraction.

Dose: 0.3-0.5 ml of 1:1000 soln IM

Indications of Adrenaline
2. Control of haemorrhage
Arenaline1:10,000
Bleeding stops d/t vasoconstriction.
Tooth extraction
Epistaxis
Bleeding in mouth
Indications of Adrenaline
3. With local anaesthetics
Adrenaline 1:1,00,000

Adrenaline produces vasoconstriction &

reduces the rate of absorption of LA.

a. Prolongs the action of LA .

b. Reduces systemic toxicity.
local anaesthetics + adrenaline

Contraindicated

1. Tips of finger & toes

2. Ear lobule
3. Tip of nose
4. Tip of penis

End arteries tissue necrosis &

gangrene
Indications of Adrenaline
4. Cardiac arrest
Intracardiac adrenaline
Dipivefrine
Prodrug of adrenaline.

Stimulates α & β receptors.

Increases aqueous humor outflow.

Indication: open angle glaucoma.

Norepinephrine ( noradrenaline)
Agonist at α & β1 receptor.

IV infusion.

Extravasates local tissue necrosis.

Indication: Shock rarely used.

a. Catecholamines a. Catecholamines

b. α1,α2, β1,β2 & β3 b. α1,α2,β1& β3

c. Adm IV,IM,SC intracardiac c. Adm only IV infusion.

& topical.

d. Biphasic response. d. Biphasic response not seen

Adrenaline Noradrenaline
e. Bronchodilator e. Not seen

f. Indication f. Indication
Anaphylactic shock Shock
Control haemorrhage
Prolong action of LA

Adrenaline Noradrenaline
Dopamine
Agonist at D1, β1 & α1.
 Dopamine
Mcg/kg/min  Effects

a. 2-5 D1 a. Renal, mesentric & cerebral

vasodilatation.

b.5-10 D1+ β1 b. Same as above + increase in

myocardial contraction.

c. 11-20 β1 c. Predominantly cardiac

contraction.

d. >20 α1 d. Vasoconstriction.
Dopamine
Does not cross BBB.

Short acting & the infusion rate can be

adjusted to get the appropriate effect by
monitoring BP.

Metabolised by COMT & MAO.

Dopamine
Adverse effects
Nausea, vomiting,
Palpitation, headache,
Angina & sudden rise in BP.

Indication
Cardiogenic shock with oliguria.
Dobutamine
β1 agonist.

Increases the force of cardiac contraction

& output.

2.5-10 mcg/kg/min iv infusion.

Dobutamine
Inotropic agent in pump failure

accompanying MI,

cardiac surgery &

for short term management of severe CHF.

Isoprenaline
β agonist acts on β1 & β2 receptors.

No action on α receptor

β1 Cardiac stimulant tachycardia

β2 Vasodilatation in skeletal muscle

Bronchodilatation
 Isoprenaline
Not effective orally
Extensive first pass metabolism.

Metabolised only by COMT

Indication
1. Stimulate HR in heart block
2. Bronchial asthma replaced by β2 agonists
Ephedrine
Alkaloid obtained from ephedra vulgaris.

Mixed acting sympathomimetic.

Repeated injections produce tachyphylaxis.

Resistant to MAO therefore effective orally.

Crosses BBB causes CNS stimulation.

 Ephedrine
Indication

Nasal decongestant

Hypotension during spinal anaesthesia.

Amphetamines
Synthetic compound.

Indirect acting sympathomimetic.

Tachyphylaxis occur on repeated use.

Potent CNS stimulant.

Amphetamines
Produces increased mental & physical activity.

Alertness, increased concentration &

attention span, elation, euphoria &
increased capacity to work.

Improves performance in athletes.

Dope test

Drug of psychological dependence & abuse.

Depression of appetite acting on the feeding
centre in the hypothalamus reduces hunger &
suppresses appetite.

Adverse effect
Restlessness
Tremor
Insomnia
hallucination
 Indications
a. Attention deficit hyperactive disorder
(ADHD)
in children is characterised by decreased
ability to concentrate & hold attention,
aggressive behaviour & hyperactivity.
Indications
b. Narcolepsy
sleep disorder

Modafinil new drug

Centrally acting CNS stimulant
Acts by stimulating α1
Also affects GABA & serotonin receptors.
It is better tolerated with fewer adverse
effects.
Indications
c. Obesity
Appetite is suppressed.

Butdue to risk of dependence

amphetamine should not be used.
 Indications
d. Nocturnal enuresis in children & urinary
incontinence.

In children >5 years.

Imipramine adm at bedtime.

Phenylephrine
Selective α1 agonist.

Raises BP by causing vasoconstriction.

Orally as nasal decongestant.

Topically
a. Nasal decongestant
b. Mydriasis to facilitate fundus examination
without cycloplegia.
Nasal Decongestants

Phenylephrine – α1 agonist

Naphazoline
Xylometazoline α2 agonist
Oxymetazoline
Nasal decongestants
Stimulates α receptors present in the blood
vessels of nasal mucosa.

Bringabout vasoconstriction of the nasal

mucosa, resulting in shrinkage & decrease
volume of the mucosa.

 Thus they relieve nasal congestion &

decrease resistance to airflow through the
nose.
 Adverse Effects
Prolonged use can cause
a. Atrophy of the nasal mucosa due to intense
vasoconstriction (rhinitis medicamentosa)

b. Recongestion or after congestion may result

when the drug is stopped.
Indication
a. Rhinitis

b. Sinusitis
α2 agonistic drugs
Clonidine

α methyl dopa

Apraclonidine

Brimonidine

Tizanidine
α2 receptors
1. Presynaptically on sympathetic neurons
Decrease release of NA.

2. Postsynaptically in blood vessels

Vasoconstriction.

3. Brain decrease central sympathetic

outflow.
Indications
α methyl dopa

Hypertension during pregnancy

Indications Of Clonidine
a. Hypertension

b. Opioid withdrawal, alcohol withdrawal

&
smoking cessation.

c. Control loose motions due to diabetic

nephropathy.
Adverse effects
1. Sedation
2. Dryness of mouth
3. Bradycardia
4. Sudden withdrawal of clonidine
Rise in BP, tachycardia, sweating.
Sudden removal of central sympathetic
inhibition resulting in release of large
quantities of stored CAs.
Indications
Apraclonidine Brimonidine
Glaucoma

Tizanidine: Centrally acting skeletal

muscle
relaxants.
Selective β2 stimulants/agonists
 Bronchodilators
SABA, LABA , ULABA

 Uterine relaxants
Ritodrine Salbutamol
Isoxsuprine Terbutaline
Pharmacological actions
Smooth muscle relaxants

1. Bronchodilatation

2. Vasodilatation

3. Uterine relaxation
Adverse Effects
Muscle tremors

Tachycardia

Tolerance

Hypokalemia

Ankle edema

Hyperglycemia
INDICATIONS
1. Bronchial asthma ,COPD

2. Uterine relaxants to delay premature

labour
 Bronchodilators

A. SABA (Short acting) B. LABA (long acting)

use : symptomatic relief use: Asthma Prophylaxis
Salbutamol (albuterol) Salmeterol
Terbutaline Formoterol
Levosalbutamol Bambuterol
Fenoterol
Pirbuterol
Remiterol
Bitoterol

C. ULABA
Ultra long acting beta 2 agonists : Vilanterol, Indacaterol, Olodaterol
Mechanism of action

1. Stimulation of Beta 2 rs in bronchial smooth ms -> increases cAMP ->

reduction in smooth ms tone
2. Increased conductance of large Ca+ sensitive K+ channels in Smooth
ms which causes membrane hyperpolarisation and relaxation
3. Phospholipase A2 inhibition
4. Inh. of myosin light chain kinase activators and activate myosin light
chain phosphatase
5. Beta 2 rs are present in mast cells, basophils, eosinophils, neutrophils
and lymphocytes
Beta 2 stimulation -> signalling cascade activated -> inhibits release
of inflammatory mediators and cytokines
6. decrease in microvascular leakage
7. increase mucociliary clearance
8. inh Ach release
 SABA

Most effective in relaxing airway sm ms

Reverses bronchoconstriction
Inhalational onset: 1-5mins , action 2-6 hrs

SALBUTAMOL ( ALBUTEROL )
 highly selective beta 2 agonist
 oral BA : 50%
 inhalational onset 5 mins , action 2 – 4 hrs
 Ideally suited for acute attack of asthma
 not suitable for Px
 A/E : ms tremors, palpitations , restlessness, hypokalemia
hyperglycemia , ankle edema , throat irritation, nervousness
Dose and preparation
oral : 2-4 mg
IM, SC : 0.25 – 0.5mg
inhalational : 100 – 200 mcg (rotacaps, MDI, accuhaler)

TERBUTALINE
- similar to salbutamol
 dose: oral 5mg ; SC 0.25mg ; inhalational 250 mcg
 Tablets, syrups, MDI , nebulising solutions
 only bronchodilator which can be safely used in
PREGNANCY
 Regular use of Beta 2 agonists can cause DOWN
REGULATION
OF RECEPTORS
 LABA

SALMETEROL
 Provides sustained persistent bronchodilation
 lasts over 12hrs
 slow onset of action
 extended side chain on salmeterol makes it 10000 times more
lipophilic than salbutamol
 More beta 2 selective than salbutamol
 dose : 50 mcg BD puff , 100 mcg in severe cases

FORMOTEROL
 action for 12 hrs when inhaled
 faster onset - 10 mins
 dose: 12-24 mcg BD by inhalation
BAMBUTEROL

 prodrug of terbutaline
 single dose : 10 – 20mg tablet for chronic bronchial asthma
 action for 24 hrs

Indication for LABA

1. Nocturnal asthma
2. Exercise induced asthma
3. Initiating Rx for persistent asthma

Indication of ORAL LABA Rx : elderly , children

ANTI-ADRENERGIC DRUGS
Antiadrenergics or
Adrenergic receptor antagonists

Oppose the receptor action of epinephrine

&
other sympathomimetics.

1. Alpha antagonists

2. Beta antagonists
Alpha antagonists

1. Nonselective blocker: Phenoxybenzamine

Phentolamine
Tolazoline
Ergotamine

2. Selective α1 blocker: Prazosin

Terazosin
Doxazosin
Tamsulosin
Silodosin
Alfuzosin

3.Selective α2 blocker: Yohimbine

Shared properties of α blocker
1. α1 blockade inhibits vasoconstriction
leading to vasodilatation & fall in BP.

2. α2 blockade enhances release of NA

tachycardia.

a. Nonselective α1 blocker hypotension with

tachycardia.

b. Selective α1 blocker hypotension without

tachycardia.
Blockade of alpha receptor
3. Nasal blood vs results in nasal stuffiness.

4. Radial muscle of iris miosis.

5. Vas deferens inhibition of ejaculation.

6. Bladder trigone, spincter and prostate

causes better flow of urine & reduces
prostatic hypertrophy.
Phenoxybenzamine
Binds covalently to α1 & α2 receptors
causing irreversible blockade.

t1/2 of 24 hours.

Action lasts for 3-4 days.

Used orally in pheochromocytoma.

Phentolamine
Blocks α1 & α2 receptors.

t1/2 19 mins.

Rapid & short acting drug.

 Indications

a. Pheochromocytoma
Diagnosis & intraoperative management.

b. Extravasation of adrenergic drugs

Local infiltration to counteract vasoconstriction

c. Impotence in combination with papaverine.

d. Control hypertension due to clonidine

withdrawal.
Pheochromocytoma
Adrenal medullary tumor which secretes
large amount of catecholamines resulting in
hypertension.
The tumor has to be surgically removed .
Phenoxybenzamine & phentolamine are
used for the preoperative management of
the patient & during the operation.
Inoperable cases are put on long term
treatment with phenoxybenzamine.
Ergotamine
Non selective α blocker

Blockade is of short duration.

Vasoconstriction

Indication acute attack of migraine.

Prazosin
Selective α1 blocker.

Fall in BP without tachycardia.

Relax urinary bladder trigone, spincter &

prostatic capsule & are useful in
prostatic hypertrophy.

Decreases LDL & Triglycerides increases HDL.

Prazosin
60% BA

t1/2 2-3 hours

DOA 6-8 hours

Adverse Effects
1. First dose phenomenon After the first dose,
marked postural hypotension occurs which
may lead to fainting.

2. Palpitation.

3. Nasal stuffiness.

4. Impaired ejaculation.
Indications
1. Hypertention
1-4 mg bd/tds
(start with a low dose 0.5 mg HS)

2. BHP .

3. CHF in conjunction with diuretics & cardiac

glycosides.

4. Raynaud’s disease.
Congeners of prazosin
Longer acting can be given once daily.

Highly selective for α1 receptos.

Postural hypotension is milder.

Tamsulosin is uroselective α1A & α1D receptor

which are dominant in bladder & prostate.

Relieves the symptom of BHP .

Tamsulosin
Uroselective α1A & α1D receptor
which are dominant in bladder & prostate.

Improves urine flow rate.

Relieves the symptom of BHP .

Terazosin
>90% BA

t ½ 12 hrs

DOA 24hrs

Indication : 1. hypertension
2. BPH

Dose: 2-10 mg OD
Doxazosin
Long acting selective α1 blocker

t 1/2 18 hours.

DOA 36 hrs

Indication : 1. hypertension
2. BPH
Additional action in BHP
Terazosin & Doxazosin induces apoptosis

in prostrate smooth ms cells.

Not α1 mediated.
Tamsulosin
Selective α1 antagonist for α1A & α1D rs.

Blocks α1A rs in bladder base & prostate:

improves urine flow rate &
reduces symptoms of BHP.

t1/2 6-9 hrs

Modified release Cap for OD adm.

Indication: BHP

0.4 mg Modified release Cap OD in the morning

with meals
Silodosin , Alfuzosin
Indications of selective α1 blocker
1. Hypertension

2. CHF because of its vasodilator action, prazosin is

used. But ACE I are preferred.

3. BHP

4.Peripheral vascular diseases like

raynauds phenomenon affords symptomatic
relief.
Beta Blockers

Beta adrenergic blocking drugs

Block the action of catecholamines

mediated
through the β receptor.
Classification
I.Generation 1
Nonselective beta blocker (beta 1 + beta 2)

Propranolol
Sotalol
Timolol
Pindolol
Nadolol
Classification

II. Generation II
Cardioselective β1 blocker
Atenolol Acebutalol
Betaxolol Bisoprolol
Metoprolol Esmolol
Classification

III. Generation III

a. Non selective – Carteolol, bopindolol
b. Cardioselective β1 blocker
Nebivolol , Celiprolol, betaxolol
c. Beta plus alpha blocking (additional
vasodilatory)
Carvedilol, labetalol
ISA – partial agonistic action
Carteolol, labetalol, acebutolol, pindolol

MSA
Propranolol, oxprenolol, pindolol
Pharmacological actions
1.CVS
a. Decreases HR.

b. Decreases force of myocardial contractility.

c. AV conduction is delayed.

d. Decreases BP in hypertensives.
Beta blockers as antihypertensives
a. Blocks β1 receptor in the heart

b. β1 receptor in the JG apparatus.

Decrease renin secretion.

c. Blocks presynaptic β2 receptors,

inhibits the release of NA.

d. Central action reducing sympathetic outflow.

 2. RS
Blocks β2 receptor in bronchial smooth

muscle bronchoconstriction.
3. Metabolic
a. Unfavourable lipid profile.

b. Inhibits glycogenolysis.
Hypoglycaemic unawares.
4. Skeletal muscle
a. Inhibits tremors.

b. Decrease exercise capacity by decreasing

blood flow.
 5. Eye
Reduces secretion of aqueous humour &

IOT is lowered.
 Propranolol
Non selective β blocker.

Well absorbed after oral administration.

Low oral BA due to high first pass metabolism (can be

given orally in high dose)

Lipophilic.

Dose:10 mg BD max 320 mg in 2-4 times

daily.
Cardioselective β1 blockers
1. Bronchoconstriction is less.
2. Less interference with carbohydrate
metabolism.
Tachycardia in response to hypoglycaemia is
blocked.
3. Lower incidence of cold hands & feet.
4. Less deleterious effect on blood lipid profile.
5. Ineffective in suppressing essential tremors.
6. Less liable to impair exercise capacity.
 Atenolol Metoprolol
1. Selective β1 blocker. 1. Selective β1 blocker.

2. Lipophilic crosses BBB

2. Hydrophilic d/n cross 2. Lipophilic crosses BBB
BBB
3. First pass metabolism
3. First pass metabolism 3. significant.
First pass metabolism
not significant. significant.
4. 40-50 %
4. 50-60 %
5. t1/2 6-9 hours.
5. t1/2 3-4 hours.
6. Major route of elimination
is renal. 6. Major route of elimination
is hepatic.
7. Dose: 25-50 mg OD

7. dose: 50-100 mg bd

Atenolol Metoprolol
 Timolol

Non selective β blocker.

Eye drops in open angle glaucoma.

Pindolol
Non selective β blocker.

Intrinsic sympathomimetic action on β1 & β2.

Lesser bradycardia & myocardial depression.

Less Rebound hypertension after withdrawal.

Less troublesome in asthmatics.

Esmolol
Ultrashort acting β1 blocker.

Plasma t1/2 8-10 mins.

Inactivated by esterases in blood.

IV infusion rapid onset, short lasting fall in BP

Supraventricular tachycardia.

To reduce HR & BP during & after cardiac surgery.

Labetalol
α& β adrenergic blockers.
Blocks of α1, β1& β2 receptor.

Fall in systolic & diastolic BP (α1, β1block).

Orally effective but undergoes first pass metabolism.

Indicated in hypertensive emergencies IV

1. Pheochromocytoma
2. clonidine withdrawal
Carvedilol
β1+β2+α1 blocker
α1 blockade vasodilatation
Antioxidant property
Hypertension
CHF
Dose: CHF: 3.125 mg BD X 2 Weeks
increase 25 mg BD

HT :6.25 mg BD increase 25 mg BD

Nebivolol
Selective β1 blocker + NO donor

 Produces vasodilatation.

Improves endothelial function.

Indications
1. HT
2. CHF
Drug Interactions
1. Propranolol + Verapamil
Additive depression of SA node &
AV conduction cardiac arrest.

2. Propranolol delays recovery from

hypoglycaemia due to insulin &
oral antidiabetics.

3. Propranolol retards lidocaine metabolism by

reducing hepatic blood flow.
Adverse Effects
1. CVS
Bradycardia
Hypotension
Heart block

2. RS
Bronchoconstriction
Ppt acute attack of asthma
Adverse Effects
3. CNS
Insomnia, Night mares,
Depression, Hallucination,
Forgetfulness, Confusion.

4. Skeletal muscle
Worsening of PVD, Fatigue,
Myopathy, Muscle cramps.

5. Skin rash & alopecia.

Adverse Effects
6. Metabolic
a. Hypoglycemia.
Hypoglycaemic unawares.

b. Unfavourable lipid profile.

Increases TG & LDL levels.
Decreases HDL levels.
7. Abrupt withdrawal of β blockers after
prolonged use:
Rebound hypertension & ppt anginal
attacks.
Due to upregulation of β receptors.
Hence BB should be gradually tapered.
Indications of β blockers
1. Hypertension
One of the first choice drugs
Use to treat mild to moderate hypertension.

2. Angina pectoris
BB are useful in treatment of stable angina.
Decrease cardiac work & oxygen demand.
Taken on regular schedule & not on as an
when required.
Indications of β blockers
3. Cardiac arrhythmias
Useful in treatment of both ventricular &
supraventricular arrhythmias.

4. myocardial infarction.
Acute MI limit the size of infarct.
Patients who have recovered from MI
long term treatment prolongs survival.
Indications of β blockers
5. CHF
Sympathetic system is stimulated in CHF
which is deleterious to the heart &
contribute to cardiac remodelling.
Indicated in Class II & Class III CHF.
Metoprolol, Carvedilol & Bisoprolol

6. Obstructive cardiomyopathy
Indications of β blockers
7. Pheochromocytoma
Given along with α blockers to control
hypertension.

8. Thyrotoxicosis
a. Controls symptoms due to sympathetic
overactivity like palpitations, tremors.
b. Prevents peripheral conversion of T4 to T3.
Indications of β blockers
9. Glaucoma
Timolol, Betaxolol & Levobetaxolol is used topically.

10. Prophylaxis of migraine.

11. Anxiety
Tremors tachycardia due to sympathetic overactivity
are relieved.

12. Essential tremors

13. Dissecting aortic aneurysm

Contraindications
1. Class IV CHF
Prevent sympathetic overactivity.

2. Bradycardia

3. Heart block depress AV conduction

4. Bronchial asthma & COPD.

5. Diabetes mellitus
Important topics (AHS)
Adrenergic Receptor distribution
Adrenergic agonists esp. Adrenaline,
Noradrenaline, Dopamine, dobutamine, nasal
decongestants, B2 agonists
Uses , adverse effects of adrenaline
Uses of adrenergic drugs (agonists)
Uses of alpha antagonists
Cardioselective beta blockers
Uses and a/e of beta blockers
Carvedilol, labetalol, esmolol
THANK YOU