Sympathomimetic Drugs

Sympathomimetic drugs, also known as adrenergic agonists, mimic the action of the stimulators (α, β, or dopamine receptors) of the sympathetic autonomic nervous system. Sympathomimetic drugs are classified based on the type of receptors the drugs act on (some agents act on several receptors but 1 is predominate). Clinical uses of sympathomimetics include the treatment of hypotension, asthma, and anaphylaxis. The primary drugs used as IV vasopressors in the hospital are dopamine and norepinephrine. Dobutamine is given IV as an inotrope. Albuterol is used via nebulizer or metered-dose inhaler for asthma. Sympathomimetics may produce a wide range of adverse effects, which generally resemble excessive stimulation of the sympathetic nervous system. The effects may include palpitations, tachycardia, and/or arrhythmias due to stimulation of cardiac β receptors.

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Chemistry and Pharmacodynamics

Sympathomimetic drugs, also known as adrenergic agonists, mimic the action of the stimulators of the sympathetic autonomic nervous system, specifically α, β, or dopamine receptors:

Chemical structures

  • Phenylethylamine (parent compound)
  • 4 possible substitution sites:
    • Benzene ring: substitution by a hydroxyl group (-OH) at position 3 and 4 yields catecholamine (dopamine)
    • Terminal amino group (epinephrine)
    • Α or β carbons of the ethylamino chain (amphetamine and phenylephrine respectively)

Mechanism of action

  • At the end of a neuron, terminal buttons (structures at the end of an axon) carry signals to neighboring neurons (synapses), glands, or muscles.
  • The synapses provide room for the chemical signal to travel and exert the effect.
  • Sympathomimetics affect the adrenergic receptors of epinephrine, norepinephrine, or dopamine to produce effects on α, β, or dopamine receptors.


  • Classification is based on the type of receptors the drugs act on.
  • Direct agonists (selective) act on 1 or more adrenergic (α and β) receptors:
    • Α agonists:
      • Nonselective: norepinephrine
      • Α-1 selective: phenylephrine
      • Α-2 selective: clonidine
    • Β agonists:
      • Nonselective: epinephrine, isoproterenol
      • Β-1 selective: dobutamine
      • Β-2 selective: albuterol
  • Indirect agonists: 
    • Stimulants: cause increased release of the endogenous neurotransmitter (e.g., amphetamines)
    • Tricyclic antidepressants: inhibit reuptake of neurotransmitters → “anticholinergic” side effects
  • Mixed: 
    • Employ mechanisms of both direct and indirect activation
    • Ephedrine: acts on α and β receptors to cause norepinephrine release (used for anesthesia-related hypotension)

Physiologic effects

  • Cardiovascular (e.g., epinephrine, norepinephrine):
    • Increases heart rate
    • Increases contractile force (positive inotropy)
    • Increases blood pressure by increasing total peripheral resistance
    • Isoproterenol (nonselective agent):
      • Increases cardiac output 
      • Decreases blood pressure (opposite of epinephrine)
  • Respiratory (e.g., albuterol):
    • Β-2 agonists relax smooth muscle → bronchodilation 
    • Albuterol is used for asthma.
    • Epinephrine is used for anaphylaxis.
  • Ocular:
    • Pupil dilation (mydriasis)
    • Accommodation is rarely affected.
    • Reduces intraocular pressure
  • Gastrointestinal:
    • Contracts smooth muscle in the splanchnic vessels
    • Low-dose dopamine causes vasoconstriction.
  • Renal:
    • Detrusor muscle relaxation
    • Trigone contraction
  • Genital tract (women):
    • Β-2 agonists cause uterine relaxation.
    • Terbutaline is used to suppress preterm labor.
  • Genital tract (men):
    • Α-1 agonists cause prostatic smooth muscle contraction (α blockers are used for benign prostatic hypertrophy, which causes urinary outflow obstruction).
    • Ephedrine is sometimes used for urinary incontinence.

Pharmacokinetics and Indications

The primary drugs used as IV vasopressors in the hospital are dopamine and norepinephrine. Dobutamine is given IV as an inotrope. Albuterol is used via nebulizer or metered-dose inhaler for asthma. Typical uses of certain medications include:

Routes of administration

Many routes are available:

  • Oral:
    • Midodrine (used for orthostatic hypotension)
    • Clonidine (a centrally acting antihypertensive agent)
    • Pseudoephedrine (nasal decongestant)
  • Rectal: phenylephrine (vasoconstrictor suppositories for hemorrhoids)
  • Topical: eye drops for glaucoma (α agonists reduce intraocular pressure)
  • IV (pressors for hypotension in hospitalized individuals):
    • Epinephrine
    • Dobutamine
    • Norepinephrine
  • Inhaled (for asthma):
    • Albuterol (short-acting β agonist)
    • Salmeterol (LABA)


Sympathomimetic drugs are used to augment endogenous catecholamines of the sympathetic nervous system for therapeutic benefit.:

Α-1 selective agonist phenylephrine:

  • Used as an IV vasopressor to increase blood pressure by increasing total peripheral resistance
  • Does not directly act on the heart → induces reflex bradycardia (a counter-regulatory mechanism)
  • Contracts smooth muscle in the splanchnic vessels
  • Used topically as a vasoconstrictor for nasal congestion due to allergic rhinitis

Α-2 selective agonist clonidine:

  • Decreases blood pressure by CNS accumulation → reduced sympathetic outflow
  • Not a 1st-line drug for hypertension

Β-1 selective agonist dobutamine:

  • Mostly stimulates myocardial β-1 adrenergic receptors; increases cardiac output (contractility)
  • Increases blood pressure
  • Lesser effects of α-1 and β-2 receptor agonists, greater effects of β-1 receptor activation → vasodilation in addition to the inotropic and chronotropic actions
  • Route: IV
  • Onset of action: 1–10 minutes
  • Peak effect: 10–20 minutes
  • Metabolism: tissue and hepatic (to inactive metabolites)
  • Half-life elimination: 2 minutes
  • Excretion: urine (as metabolites)

Β-2 selective agonist albuterol:

  • Use: for bronchodilation with asthma or other causes of bronchoconstriction
  • Route: inhaled or oral (rarely used)
  • Onset and duration of action:
    • Nebulizer solution: ≤ 5 minutes, lasts 3–6 hours
    • Oral inhaler: 5–8 minutes, lasts 4–6 hours
  • Metabolism: hepatic
  • Excretion: 80% urine, 20% feces

Nonselective dopamine:

  • Works on different receptors at different doses:
    • Low dose: dopamine receptors
    • Intermediate dose: β receptors
    • High dose: α receptors
  • Route: IV
  • Onset of action:
    • Adults: within 5 minutes
    • Neonates and children: ≤ 1 hour
  • Duration in adults: < 10 minutes
  • Metabolism: 
    • Renal, hepatic, and plasma
    • 75% to inactive metabolites by MAO, 25% to norepinephrine (active)
  • Half-life elimination: approximately 2 minutes (excreted in the urine)

Mixed α-/β-agonist epinephrine:

  • Indications: 
    • Use SC for anaphylaxis and type 1 IgE-mediated reactions.
    • Use IV for hypotension in septic shock.
  • Onset of action for bronchodilator (SC): approximately 5–10 minutes
  • Distribution: does not cross the blood-brain barrier
  • Metabolism: taken into the adrenergic neuron and metabolized by MAO and catechol O-methyltransferase (COMT) (the circulating drug undergoes hepatic metabolism)
  • Route: IV
  • Half-life elimination: < 5 minutes
  • Excretion: urine 
  • Used in advanced cardiac life support (ACLS) protocol for:
    • Sudden cardiac arrest due to asystole
    • Pulseless electrical activity
    • Ventricular fibrillation
    • Pulseless ventricular tachycardia

Mixed α-/β-agonist norepinephrine:

  • Indications: severe hypotension/shock
  • Α effects (vasoconstriction → blood pressure and coronary blood flow) > β effects (inotropic and chronotropic effects)
  • Duration (vasopressor): 1–2 minutes
  • Protein binding: 25% mainly albumin
  • Mean half-life elimination: approximately 2.4 minutes
  • Time to peak steady state: 5 minutes
  • Excretion: urine
  • Metabolism: short duration of action due to:
    • Rapidly metabolized by COMT and MAO
    • Readily taken up into the nerve endings

Adverse Effects and Contraindications

Sympathomimetics may produce a wide range of adverse effects resembling excessive stimulation of the sympathetic nervous system, including palpitations, tachycardia, and arrhythmias due to stimulation of cardiac β receptors.

Adverse effects

  • Due to excessive adrenergic receptor activity
  • IV extravasation of potent vasoconstrictors can cause local ischemia (central line is preferred).
  • Α-1 agonists (e.g., phenylephrine, norepinephrine):
    • Hypertension
    • Reflex bradycardia
    • Piloerection
    • Urinary retention
    • Vasoconstriction: may produce distal ischemia and necrosis
  • Α-2 agonists (e.g., clonidine):
    • Sedation
    • Respiratory depression
    • Bradycardia
    • Hypotension and shock
    • Miosis
    • Rebound hypertension
    • Xerostomia 
  • Β-1 agonists (e.g., dobutamine):
    • Tachycardia/arrhythmias
    • High-dose IV → can cause mesenteric ischemia 
    • Acute coronary syndrome in individuals with underlying coronary artery disease
  • Β-2 agonists (e.g., albuterol, salmeterol):
    • Tremors
    • Agitation
    • Insomnia
    • Tachycardia
    • Hyperinsulinemia
    • Hyperglycemia
    • Hypokalemia

Drug-drug interactions

  • Βeta blockers: may antagonize the effects of β agonists → diminish the therapeutic effect
  • Cannabinoid products: may enhance the tachycardic effect of sympathomimetics
  • Stimulants (e.g., caffeine, amphetamines): may enhance the adverse/toxic effect of sympathomimetics
  • Α-1 blockers (e.g., doxazosin, tamsulosin): 
    • May diminish the vasoconstrictive effect of dopamine
    • Dopamine may antagonize α-1 blocker vasodilation.
  • Serotonin-norepinephrine reuptake inhibitors (SNRIs): 
    • May enhance the tachycardic and vasopressor effects of α and β agonists
    • If coadministered → monitor for increased sympathomimetic effects (e.g., hypertension, chest pain, or headache)
  • Tricyclic antidepressants: 
    • May enhance the vasopressor effect of the α and β agonists (avoid combining if possible)
    • Monitor for evidence of increased pressor effects and consider reductions in initial dosages of the α and β agonists.

Contraindications for clinical use

  • Sympathomimetics should be used with caution in individuals with cardiovascular disorders; however, many are used in life-threatening situations.
  • Specific contraindications to certain agents:
    • Extreme bradycardia (phenylephrine)
    • Hypertrophic obstructive cardiomyopathy (dobutamine)
    • Heart failure (isoproterenol)

Comparison of Medications

Table: Commonly used sympathomimetic drugs
SubclassMechanism of actionEffectsClinical applicationsPharmacokinetics, toxicities, interactions
Α-1 agonists (midodrine, phenylephrine)Activates phospholipase C → increased intracellular calcium and vasoconstrictionVascular smooth muscle contraction → increases blood pressureOrthostatic hypotension
  • Oral administration
  • Peak effect: 1 hour
  • Toxicity: hypertension, piloerection (goosebumps), and urinary retention
Α-2 agonists (clonidine)Stimulates α-2 adrenoceptors in the brain stem → reduced sympathetic outflowVasoconstriction is masked by the central sympatholytic effect → lowers blood pressureHypertension
  • Oral, transdermal
  • Peak effect: 1–3 hours
  • Half-life of oral drug: approximately 12 hours
  • Produces xerostomia and sedation
Β-1 agonists (dobutamine)Activates adenylyl cyclase (increases myocardial contractility)Positive inotropeCardiogenic shock and acute heart failure
  • IV administration
  • Requires dose titration to the desired effect
Β-2 agonists (albuterol)Activates adenylyl cyclaseBronchial smooth muscle dilationAsthma
  • Administration via inhalation
  • Duration: 4–6 hours
  • Toxicity: tremor and tachycardia


  1. Horowitz, A. J., Smith, T., & Frey, D. (2021). Sympathomimetics. StatPearls. Retrieved September 24, 2021, from
  2. Kanter, J., & DeBlieux, P. (2014). Pressors and Inotropes. Emergency medicine clinics of North America. 32(4), pp. 823–34.
  3. Manaker, S. (2020). Use of vasopressors and inotropes. UpToDate. Retrieved September 24, 2021, from
  4. Lexicomp, Inc. (2021). Albuterol (salbutamol): Drug information. UpToDate. Retrieved September 29, 2021, from
  5. Lexicomp, Inc. (2021). Norepinephrine: Drug information. UpToDate. Retrieved September 29, 2021, from
  6. Lexicomp, Inc. (2021). Dopamine: Drug information. UpToDate. Retrieved September 29, 2021, from
  7. Lexicomp, Inc. (2021). Dobutamine: Drug information. UpToDate. Retrieved September 29, 2021, from

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