Type
Subtype
Name
Mechanism of
action
Effect
Theraputic
use
ADR
Extra
Adrenergic
agonist
Direct
Non-selective
Epinephrine
α1, α2, β1, β2
Bind to adrenergic
receptors  SNS
activity.
CVS:
*β1-↑Chronotropic and
inotropic effects
*β2-vasodilation in muscles.
*α1-vasoconstriction.
*systolic↑ diastolic ↓.
Bronchidialtion(β2)
Hyperglycemia:
*insulin↓ (α2)
*gluconeogenesis(β2)
Lipolysis (β3)
*Cerebral
hemorrhage.
*Arrhythmias.
*Anxiety.
*Tremors.
*Headaches.
*Pulmonary edema.
*Rapid inactivation
by COMT & MAO.
*Poor penetration
to CNS due to
polarity.
Adrenergic
agonist
Direct
Non-selective
Norepinephrine
α1, α2, β1
Bind to α1, α2, β1
receptors
CVS  ↑systolic & diastolic
*no β2 for vasodilation.
* β1↑intropic effect.
*α1↑peripheral resistance.
*Anaphylectic shock.
*Cardiac errest.
*Stop bleeding.
(vasoconstriction)
*Prolong anesthesia.
*Open eye glaucoma
(α1 ↓aqueous
humor production
through
vasoconstriction of
ciliary body blood
vessels).
*Hypotension.
*Septic shock.
*Arrhythmias.
*↑BP
*Tissue necrosis.
*Vasospasms.
*Rapid inactivation
by COMT & MAO.
*Poor penetration
to CNS due to
polarity.
Adrenergic
agonist
Direct
Non-selective
Isoproterenol
β1, β2
Bind to β1, β2
receptors.
CVS:↑diastolic & systolic
moderately.
*β1-↑Chronotropic and
inotropic effects.
*β2-vasodilation in muscles.
Bronchidialtion(β2)
*Bradycardia.
*AV block.
*Asthma (rare).
Adrenergic
agonist
Direct
Selective
α2
Apraclonidine
Bind to α2 receptors
(imidazole type).
Act on ocular α2 receptors
(inhibit ciliary epithelium 
aqueous humor
production↓)
Glaucoma
*Cerebral
hemorrhage.
*Arrhythmias.
*Anxiety.
*Tremors.
*Headaches.
*Pulmonary edema.
negligible
Adrenergic
agonist
Direct
Selective
β2
-Terbutaline
-Salmeterol
-Albuterol
Bind to β2 receptors.
Bronchodilation
T&A: Acute
bronchospasm &
COPD.
S: nocturnal
bronchospasm.
*Hyperglycemia.
*Tremor & anxiety.
*Tachycardia &
arrhythmias (can also
stimulate a bit of β1).
*Not inactivated
by COMT and poor
inactivation by
MAO.
*Penetrate to CNS
due lipophilicity.
*Administration:
topical ocular
*Doesn’t
penetrate BBB.
T&A:
oral/SC/inhalation,rapi
d onset, last for 3-6
hours.
S: powder inhalation,
longer onset, long
duration (more than 12
hours).
Type
Subtype
Name
Mechanism of action
Effect
Theraputic
use
ADR
Extra
Adrenergic
agonist
Direct
Selective
α2
Clonidine
Bind to α2 receptors
(imidazole type).
*CNS: bind to locus
ceruleus  ↓BP.
*SNS: ↓ NE release
from postganglionic
sympathetic nerves.
*PNS: ↑ tone.
Direct
Selective
β1
Dobutamine
Bind to β1 receptors.
↑ Chronotropic and
inotropic effects.
*Hypotension.
*Dry mouth.
*Sedation.
*Sexual dysfunction.
*Bradycardia.
*Withdrawal (after long
use).
*Arrhythmias.
*Do not metabolize
by COMT  long
action.
*Oral / IV.
Adrenergic
agonist
*Hypertension.
*Rehab from
opoids (act on
receptors which
produce
morphine-like
effects).
*Cardiogenic
shock.
*Acute HF.
Adrenergic
agonist
Direct
Selective
α1
Phenylephrine
Bind to α1 receptors.
*↑ peripherial
resistance, DBP, SBP
 may induce reflax
bradycardia.
*Mucous
vasoconstriction.
*Hypotension.
*Supraventricul
ar tachycardia.
*↓ Nasal&
ocular
congestion.
*Cause
mydriasis.
*Hypertension.
*Stroke.
*HF.
*Mixed acting
(direct + indirect)
*Non-selective
(D1&D2 >β>α)
Dopamine
Small: SBP ↑ (DBP
no change).
Medium: ↑HR
Large: constriction
of BV  ↑
peripheral
resistance.
*cardiogenic &
septic &
hypovolemic
shocks
(dopamine has
also receptors in
the kidney 
cause
vasodilation 
don’t damage it)
*Hypertension.
*Arrhythmia.
*Nausea.
Adrenergic
agonist
Small dose (D&β2): renal
vasodilation.
Medium dose (D&β): ↑
Chronotropic and inotropic
effects.
Large dose (D&β&α1):
vasoconstriction.
↑ NE release from
adrenergic neurons.
*Doesn’t metabolize
by COMT, only by
MAO & in the liver
 longer life span.
Type
Subtype
Name
Mechanism of action
Effect
Theraputic
use
ADR
Extra
Adrenergic
agonist
*Mixed acting
(direct + indirect)
*Non-selective
Ephedrine
Activate adrenergic receptors.
*↑SNS.
*Constrict BV and
↑HR  DBP&SBP ↑
*Bronchodilation.
*Slight stimulation
of CNS (↑vigorous)
*Tachycardia.
*BP ↑.
*Insomenia.
*Urinary retention.
Lipid soluble 
penetrate the CNS
and absorbed well in
the intestine.
Adrenergic
agonist
Indirect –
releasing agent
Amphetamine
*Stimulate intracellular
secretion of catecholamines
from vesicles.
*Competitive inhibitor of
catecholamine reuptake by
DAT & NET.
 ↑ Cateocholamis in the
synaptic cleft.
Replace stored
catecholamines.
*CNS stimulation.
*Vadoconstriction
 ↑BP.
*↑ HR.
*Bladder sphincter
constriction.
*Pseudoephedri
ne – mixture for
nasal, sinus and
eustachian
congestion.
*Methampheta
mine (illegal)
*ADD
*Urinary
incintinence.
*Anorexiant.
*Narcolepsy.
↑BP
Non
*Hypertension.
*Arrhythmia.
*Stroke.
*Drug of abuse –
addiction.
*Seizures.
*Mucous ischemia and
necrosis.
*Hypertension.
*Arrhythmia.
Adrenergic
agonist
Indirect –
releasing agent
Tyramine
Adrenergic
agonist
Indirect –
reuptake inhibitor
Cocaine
Block NET&DAT  no
reuptake of dopamine & NE.
*Vasoconstriction.
*↑BP.
*Local
anesthesia.
Adrenergic
antagonist
Inhibitor of
adrenergic
transmission
Metyrosine
Competitive inhibitor of
tyrosine hydroxylase  ↓
production of catecholamines.
↓ production of
catecholamines.
*Pheochromacy
toma.
*Control
dyskinesia.
*Hypertension.
*Addictive.
*Aggression.
*Paranoia.
*Act mainly in the
CNS.
*Oral / parental
*Inactivated by
MAO in the GIT &
Liver.
*Tyramine is found
in foods: cheese,
banana & Chianti
red wine.
Type
Subtype
Name
Mechanism of action
Effect
Theraputic
use
ADR
Adrenergic
antagonist
Inhibitor of
adrenergic
transmission
Reserpine
Inhibit VMAT irreversibly 
catecholamines are not being
kept in vesicles  degradation
by MAO.
↓ SNS tone
*Hypertension.
Severe depression.
Adrenergic
antagonist
Inhibitor of
adrenergic
transmission
Guanethidine
Displace with NE inside
vesicles  NE depletion (only
in neuron terminals, and not in
all CNS)  destroy adrenergic
neurons.
*↓Vasoconstriction.
*↓ HR
Hypertension
*Hypotension.
*Sexual dysfunctions.
*Diarrhea.
*Nasal congestion.
Adrenergic
antagonist
Non-selective α
blockers
Phentolamine
Competitive antagonist of α
receptor.
↓ Vasoconstriction
 ↓ BP.
*Pheochromacy
toma.
*Antidote for α
agonists.
*Reflex tachycardia (↓ α2
also).
*Postural hypotension.
*Sexual dysfunction.
*Vertigo.
Adrenergic
antagonist
Non-selective α
blockers
Phenoxybenzami
ne
Irreversible (covalent) binding
to α receptor.
↓ Vasoconstriction
 ↓ BP.
*Pheochromacy
toma.
*Raynaud’s
phenomenon
(arterial
spasms)
*Reflex tachycardia (↓ α2
also).
*Postural hypotension.
*Sexual dysfunction.
*Vertigo.
Adrenergic
antagonist
Non-selective β
blockers
Propranolol
Competitive antagonist of β
receptor.
*↓ Chronotropic
and inotropic effects
 O2 demend ↓.
*BP ↓
*↓ Renin secretion.
*Hypertension.
*Thyrotoxicosis
(cause high BP)
*Angina
pectoris.
*Pheochromacy
toma.
*Acute MI.
*Tremor.
*Anxiety.
*Migraine.
*Glaucoma
*Angina
pectoris.
*Hypertension.
*Migraine.
*Bronchospasm.
*Sexual impairment.
*CNS sedation.
*AV block.
*HF.
*Cold hands.
*Fatigue.
Adrenergic
antagonist
Non-selective β
blockers
Timolol
Competitive antagonist of β
receptor.
*↓ Chonotropic and
intropic effects 
O2 demend ↓.
*↓ Renin secretion.
*↓ IOP
*AV block.
*HF.
*CNS sedation.
*Bronchospasms.
*Cold hands.
Extra
*Oral / topical.
*2 hours half life
(short).
*Oral/IV
*Half-life: 4 hours.
Type
Subtype
Name
Mechanism of action
Effect
Theraputic
use
ADR
Extra
*Fatigue.
*Bradyarrhythmia.
*Hypotension.
*Fatigue.
*oral
*5-8 hours effect
*Low lipid soluble.
Adrenergic
antagonist
Selective β1
blockers
Atenolol
Competitive antagonist of β1
receptor.
*↓ Chronotropic
and inotropic effects
 O2 demand ↓.
*BP ↓
*Angina
pectoris.
*Acute MI.
*Hypertension.
Adrenergic
antagonist
Selective β1
blockers
Esmolol
Competitive antagonist of β1
receptor.
*↓ Chronotropic
and inotropic effects
 O2 demand ↓.
*BP ↓.
*Thyrotoxic
crisis.
*Acute
supraventricular
tachycardia.
*Bradyarrhythmia.
*Hypotension.
*Fatigue.
Adrenergic
antagonist
Non selective
α&β blockers
Labetalol
Competitive antagonist of α&β
receptor.
↓ in BP:
*Vasodilation.
*↓ Chronotropic
and inotropic
effects.
↓ in BP:
*Vasodilation.
*↓ Chronotropic
and inotropic
effects.
↑ CO (in HF
patients).
*Hypertensive
emergencies.
*Hypotension.
*Bronchoconstriction.
*Hepatic injury.
Adrenergic
antagonist
Non selective
α&β blockers
Carvediol
Competitive antagonist of
α&β1 receptor.
*Hypertension.
*HF.
*Bradyarrhythmia.
*Hypotension.
*Fatigue.
*IV
*Low lipid soluble.
*Very fast onset.
Oral / IV
*Oral
*Very short half
life (10 min)