This document summarizes the effects of sympathomimetic drugs. It describes how these drugs act on various receptors in the cardiovascular system, respiratory system, gastrointestinal tract, genitourinary tract, eyes, and metabolism. It provides examples of direct-acting agonists like adrenaline and noradrenaline, indirect-acting agonists like tyramine and amphetamine, and mixed agonists like ephedrine. It discusses the therapeutic uses and adverse effects of various sympathomimetic drugs.

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Sympathomimetic drugs
The general effects of sympathomimetic drugs
C.V.S Heart (β1 receptor)
1) ↑ Contractility (+ ve Inotropic effect)
2) ↑ Heart rate (+ ve Chronotropic effect)
3) ↑ Conductivity (+ ve Dromotropic effect)
Blood vessels
1) α1  V.C of B.V of skin and mucous membrane, kidney, GIT
2) β2  V.D of B.V of skeletal muscle, liver
Respiratory system β2  Bronchodilatation
GIT  Sphincter part  α  Contract
 Non sphincter part  α & β  Relaxes

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Genitourinary tract
 Bladder
 Sphincter α1 contract sphincter urinary continence
 Detrusor muscle β2 relaxation
 Men  α1 prostatic smooth muscle contraction
 Women Uterus α1 Contraction
β2 Relaxation
Eye
 α1 Contraction of radial muscle (dilator pupillary muscle) Active
mydriasis
 β ↑ Aqueous humor production

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1) Direct acting agonist
 E.g. Adrenaline & Noradrenaline
Act directly on α & β receptors
2) Indirect acting agonist
 E.g. Tyramine, Amphetamine
a)Releasers
b)Reuptake inhibitors
3) Mixed action agonists (dual
mechanism) E.g. Ephedrine
Stimulate adrenoreceptors
directly and releasing NE
Types of sympathomimetic

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Direct sympathomimetic
1) Adrenaline (Epinephrine)
Stimulate α1, α2, β1, β2 , β3
 Low doses  β2 (affinity) effects predominate  VD of vascular system
 High doses  α1 (affinity) effects predominate  VC of vascular system
Pharmacokinetics
 Absorption
 Ineffective orally rapid destruction by digestive enzymes and liver
metabolism
 Slow with S.C  because the drug causes local vasoconstriction.
 More rapid after I.M due to vasodilatation (β2 effect).
 Can be given I.V but must be used with caution to avoid cardiac arrhythmia (cardiac
fibrillation).

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Pharmacological action of adrenaline
C.V.S Heart (β1 receptor)
1) ↑ Contractility (+ ve Inotropic effect)
2) ↑ Heart rate (+ ve Chronotropic effect)
3) ↑ Conductivity (+ ve Dromotropic effect)
Blood vessels
1) α1  V.C of B.V of skin and mucous membrane, kidney, GIT
2) β2  V.D of B.V of skeletal muscle, liver
Blood pressure
 ↑ COP ↑ systolic blood pressure but
 Unchanged diastolic BP (↑ in large dose)
Respiratory system β2  Bronchodilatation
GIT  Sphincter part  α  Contract
 Non sphincter part  α & β  Relaxes

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Genitourinary tract
 Bladder
 Sphincter α1 contract sphincter urinary continence
 Detrusor muscle β2 relaxation
 Men  α1 prostatic smooth muscle contraction
 Women Uterus α1 Contraction
β2 Relaxation
Eye
 α1 Contraction of radial muscle (dilator pupillary muscle) Active
mydriasis
 β ↑ Aqueous humor production

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Metabolic
actions
Hyperglycemia due to
a) ↑ Glycogenolysis in liver (β2)
b) ↑ Glucagon release (β2)
c) ↓ Insulin release (α 2)
↑ Lipolysis (↑ free fatty acid in blood) (β3)
β3 ↑Gs ↑CAMP↑ lipase enzyme hydrolyzes TGs free
fatty acid + glycerol
Therapeutic uses
1) Bronchospasm
Adrenaline is the drug of choice in treatment of acute asthma and anaphylactic
shock, when bronchoconstriction has resulted in diminished respiratory exchange)
2) Hypersensitivity reaction such as Anaphylaxis shock
3) Cardiac arrest to restore cardiac rhythm
4) Adrenaline is add to local anesthetics to
Prolong their action, by producing VC at site of injection
5) Local hemostatic, to stop hemorrhage from the nasal mucosa

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Adverse effects of adrenaline
1) CNS disturbance (not direct effect on CNS) Anxiety, tension, tremors
and headache
2) Cardiac arrhythmia
3) Adrenaline can induce pulmonary edema (due to VC of Pulmonary B.V
 edema
4) ↑ Doses of Adrenaline may cause a sharp rise in blood pressure 
cerebral hemorrhage.
Contraindications & interaction of adrenaline
1) Diabetes (Adrenaline ↑ release of endogenous stores of glucose hyperglycemia)
So in the diabetic ↑ Insulin dose
3) β blocker Block β receptor only leaving α receptor unblocked
So β blocker prevent adrenaline effects on β receptors so adrenaline act only
on α VC ↑ PR ↑ BP

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Self Assessment
1) Interaction of adrenaline & cocaine
2) Contraindication of adrenaline in hyperthyroid patient

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2) Noradrenaline (NA or NE)
NTs of adrenergic neurons
α1, α2, β1 > β2
C.V.S
1)Vasoconstriction
 VC of most vascular beds including kidney (α1)↑PR
 ↑ Systolic and diastolic blood pressures
 NE causes greater VC than E (because NE not cause β2
VD compansation)
oE stimulate α1 VC & stimulate β2 VD
(Compensate α )
oNE stimulate α1 VC not act β2 (NO
compensation ) cause more VC

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1)Reflex Bradycardia
α1 stimulation VC↑ BP Stimulating baroreceptors reflex
stimulate to vagus  Reflex bradycardia 
 Sufficient to counteract the local actions of NE on the heart rate
 But doesn’t affect the positive inotropic effect of the drug
Therapeutic uses
NA is used to treat shock & Severe hypotension Because it ↑ Blood
pressure
o However, dopamine is better, because it does not ↓ blood flow to the
kidney as NA
It is never used for
1)Asthma (Because NA not affects β2 receptors)
2)In combination with local anesthetics
NE is a potent VC  extravasation (discharge of blood from vessel
into tissue)

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Adverse effects
 Similar to epinephrine in addition
NE may cause Blanching & Sloughing of skin (due to extreme VC
3) Isoprenaline (Isoproternol)
Stimulates β1 & β2 receptors Non selective
Pharmacological actions
C.V.S 1) Heart  ↑ all cardiac Properties
1) B.V  V.D of coronary & skeletal muscles (β2 )
Blood pressure  Hypotension
Respiratory system Bronchodilatation (β2 )
Therapeutic uses of isoprenaline
1) Heart block
2) Bronchial asthma

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4) Dopamine (intropin)
Activates D1, β1 & α1 receptors
 Drug of choice for D1 receptor
 Given by I.V. infusion because T1/2 is short (about 2 min).
 Binds to dopaminergic receptors (Gs) in mesenteric & renal vascular beds 
↑CAMP ↓ MLCK ↓ interaction between actin & myosin VD
C.V.S Stimulate β1 receptor ( heart) ↑ HR & FOC ↑ COP
At high doses  stimulates α1 receptors in B.V V.C↑ PR
Renal Activate D1 receptors (renal artery) VD  ↑ blood flow to
the kidney

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Therapeutic uses
1)Congestive heart failure (CHF)
2)Cardiogenic shock (Drug of choice)
3)Hypovolemic shock (Drug of choice)
5) Dobutamine (Selective β1 agonist)
 Doesn’t stimulate dopaminergic receptors
 ↑ AV node conduction velocity with little change in heart rate.
 Major advantage over other sympathomimetic drugs 
Doesn’t elevate oxygen demands of the myocardium,
 Given by I.V infusion to treat congestive heart failure (CHF)

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7) Phenylephrin (prefrin, Afrin)
Selective α 1 agonist
6) Oxymetazoline (α1 & α2 agonist )
 Therapeutic uses
1)Nasal decongestant
2)Relief of redness of the eyes associated with swimming, cold, or
contact lens (ophthalmic drops)
 Induces reflex bradycardia when given parentrally (No direct effect on heart )
 Used as Nasal decongestant & Mydriatic
 Adverse effects (Large doses) 
1) Hypertensive headache
2) Cardiac irregularities

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8) Methoxamine (Selective α1 agonist)
Direct acting, stimulate α1 receptors in arterioles ↑BP ↑ PR
Therapeutic uses
1) Relief attacks of supraventricular tachycardia
(Because of its effects on the vagus nerve)
2) Overcome hypotension during surgery involving halothane anesthetics
9) Selective α2 Agonists (Clonidine , Brimonidine )
Clonidine
Activate central α2 receptors ↓Sympathetic VMC  ↓sympathetic
outflow to the periphery ↓BP
Therapeutic uses:
1)Essential hypertension (↓ BP because its action ON CNS)
2)↓ withdrawal symptoms from opiates

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Adverse Effects
 Bradycardia , Dry mouth , Sedation
Brimonidine
Selective α 2 agonist ocularly ↓IOP in open angle glaucoma
1)↓ Aqueous humor production
2)↑ Aqueous humor outflow

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10) Selective ß2 agonists (little effect on heart)
 Smooth muscle  Relaxation (bronchioles & uterus )
A)Bronchodilator
Short acting bronchodilator
Salbutamol
Terbutaline,
Pirbuterol
Long acting bronchodilator
Salmeterol (Slower onset of action)
Formoterol
 Administered by metered dose inhaler.
 Bronchodilation with less cardiac
stimulation
 Single dose inhalation
 Sustained bronchodilation over 12 hrs
 Drug of choice for nocturnal asthma
 These drugs are highly efficacious
when combined with a corticosteroid

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B) Tocolytics (Uterine relaxant)
Ritodrine
↓ Uterine contractions in premature labor.
B) Indirect acting adrenergic agonists
1) Amphetamine
 Stimulates both α and β receptors
 Acts indirectly by releasing catecholamine
 Has marked CNS action
Therapeutic uses of amphetamine
a) Anorexigenic (↓Feeding center of hypothalmus)
b) Analeptic (↑ stimulate R.C)
c) Narcolepsy (sudden attach of sleep)
d) Attention-deficit hyperactivity syndrome (ADHS)
(Hyperactive children lacking the ability to be involved in any activity for longer than
few minute)

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Tyramine (not clinically useful drug)
 Found in fermented foods such as ripe cheese.
 Act indirectly to release NE.
 Metabolized by MAO.
 MAO inhibitors (e.g. Phenelizine) prevent destruction of tyramine hypertensive crisis.
Tyramine can enter the nerve terminal displace stored noradrenalinestimulate adrenoreceptors
Normally it is oxidized by MAO in the GUT but if the patient is taking MAO inhibitor can lead to serious
vasopressor episodes (hypertensive crisis).
Mixed acting adrenergic agonists
Ephedrine
 Stimulate both α and β receptors
 Obtained naturally from ephedra plant or synthetically
 CNS stimulation make it a drug of abuse

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2) Metaraminol
 It has no C.N.S. stimulant effect
 It is used to treat acute hypotension
Therapeutic uses of ephedrine
1) Nocturnal enuresis
2) Mydriatic
3) Heart block
4) Nasal decongestant
5) Bronchial asthma (Bronchodilators)
3) Cocaine
 CNS stimulant
 Drug of abuse
 It inhibits neuronal reuptake of NE Accumulate NE in synapse ↑ sympathetic
activity as well as potentiation of action of EPI and NE