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Modules Breakdown

Module	Review Articles	Video Lectures	Practice Questions	Flashcards
Psychopharmacology	8	8	21	35
Immune System Pharmacology	2	2	8	20
Nervous Pharmacology	8	7	21	50
Antimicrobials	10	9	45	110
Hematology Pharmacology	9	9	30	50
Musculoskeletal Pharmacology	1	1	7	10
Reproductive Pharmacology	2	2	16	12
Endocrine Pharmacology	2	2	20	15
Renal Pharmacology	2	2	19	20
Gastrointestinal Pharmacology	1	1	15	20
Cardiovascular Pharmacology	3	2	52	54
Respiratory Pharmacology	1	1	18	20
General Pharmacology	11	18	45	110

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Sample Summary page

Adrenergic Agonists

Writer: Mustafa A. Shahrori, MD

Keywords: Sympathomimetics, adrenergic receptors, α-receptors, β-receptors, vasopressors, bronchodilators, catecholamines, cardiovascular effects, sympathetic nervous system

Overview

Adrenergic agonists are drugs that mimic the effects of sympathetic nervous system stimulation by activating adrenergic receptors (α1, α2, β1, β2, β3) or dopamine receptors (D1, D2). These agents are classified as direct-acting (binding directly to receptors) or indirect-acting (increasing endogenous catecholamine availability). Their clinical applications span cardiovascular, pulmonary, and other systems based on their receptor selectivity profiles.

Adrenergic Receptor Classification and Neurotransmission

Adrenergic receptors (α₁, α₂, β₁, β₂, β₃) mediate effects like vasoconstriction, bronchodilation, and increased heart rate. The response to adrenergic agonists depends on receptor selectivity.

Adrenergic neurotransmission involves NE synthesis, storage (via VMAT), release, receptor binding, reuptake (via NET), and metabolism (by MAO and COMT).

For a detailed overview, refer to the article on Autonomic Receptors and Their Effects.

Direct sympathomimetics

Directly bind to and activate adrenergic receptors

Table 1: Direct-acting sympathomimetics: Receptor selectivity, Hemodynamic effects and applications

Drug	Receptor Selectivity	Hemodynamic changes	Applications
Albuterol, salmeterol, terbutaline	β₂ > β₁	↔/↑ HR (little effect)	Albuterol for acute asthma/COPD. Salmeterol for long-term asthma/COPD. Terbutaline for acute bronchospasm and tocolysis.
Dobutamine	β₁ > β₂, minimal α	↔/↓ BP, ↑ HR, ↑↑ CO	Cardiac stress testing, acute decompensated heart failure with cardiogenic shock (inotrope)
Dopamine	D₁ = D₂ > β > α (dose-dependent)	↑ BP (high dose), ↑ HR, ↑ CO	Unstable bradycardia, shock; inotropic and chronotropic effects at lower doses via β effects; vasoconstriction at high doses via α effects
Epinephrine	β > α (dose-dependent)	↑ BP (high dose), ↑ HR, ↑ CO	Anaphylaxis, asthma, shock, open-angle glaucoma; α effects predominate at high doses
Fenoldopam	D₁	↓ BP (vasodilation), ↑ HR, ↑ CO	Postoperative hypertension, hypertensive crisis. Vasodilator (coronary, peripheral, renal, splanchnic). Promotes natriuresis.
Isoproterenol	β₁ = β₂	↓ BP (vasodilation), ↑↑ HR, ↑↑ CO	Electrophysiologic evaluation of tachyarrhythmias. Can worsen ischemia. Has negligible α effect.
Midodrine	α₁	↑ BP (vasoconstriction), ↓ HR, ↔/↓ CO	Autonomic insufficiency and postural hypotension. May exacerbate supine hypertension.
Mirabegron	β₃	Minimal hemodynamic effects	Urinary urgency or incontinence, overactive bladder. Think "mirab3gron."
Norepinephrine	α₁ > α₂ > β₁	↑↑ BP, ↔ HR (may have minor reflexive change), ↔/↓ CO	Hypotension, septic shock.
Phenylephrine	α₁ > α₂	↑ BP (vasoconstriction), ↓ HR, ↔/↓ CO	Hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestant), ischemic priapism.

Abbreviations. HR: Heart rate, BP: Blood pressure, CO: Cardiac output, COPD: Chronic obstructive pulmonary disease, HF: Heart failure, HTN: Hypertension, D₁, D₂: Dopamine receptors, α, β: Alpha and beta adrenergic receptors

The distribution of adrenergic receptors varies significantly between tissues. This forms the basis for the therapeutic specificity of different sympathomimetic drugs. β₁-receptors are predominantly found in cardiac tissue, while β₂-receptors are predominantly in bronchial and vascular smooth muscle.

ALERT:

Epinephrine vs. Norepinephrine

● Epinephrine: Stronger β2 effects, useful in anaphylaxis and cardiac arrest

● Norepinephrine: Stronger α effects, better for maintaining blood pressure in septic shock

Dopamine dose-dependent effects

● Low dose (1-5 μg/kg/min): D1 effects → renal vasodilation

● Moderate dose (5-10 μg/kg/min): β1 effects → inotropic and chronotropic

● High dose (>10 μg/kg/min): α effects → vasoconstriction

Albuterol vs. Salmeterol

● Albuterol: Short-acting (4-6 hours), used for acute symptoms

● Salmeterol: Long-acting (12+ hours), used for maintenance therapy

NOTE: Remember the reversal of epinephrine's pressor effect after α-blockade (becomes depressor due to unopposed β2-mediated vasodilation), while phenylephrine's pressor effect is only suppressed but not reversed after α-blockade (Figure 1).

Figure1. Effects of epinephrine on blood pressure in the presence of adrenergic Receptor antagonists. Two line graphs depict changes in blood pressure following epinephrine administration under different receptor blockade conditions.

Indirect Sympathomimetics

Increase synaptic norepinephrine by various mechanisms

Table 2: Indirect-acting sympathomimetics: Mechanisms and Applications

Drug	Mechanism	Applications	Notable effects
Amphetamine	Releases stored catecholamines, reuptake inhibitor	Narcolepsy, obesity, ADHD	High abuse potential, increases alertness, decreases appetite
Cocaine	Reuptake inhibitor	Topical anesthesia (limited medical use)	Causes vasoconstriction, local anesthesia, euphoria. Contraindicated with β-blockers (unopposed α₁ activation)
Ephedrine	Releases stored catecholamines, some direct effects	Nasal decongestion, urinary incontinence, hypotension	Less potent than direct-acting agents, longer duration of action
Pseudoephedrine	Similar to ephedrine but with less CNS effects	Nasal decongestion	OTC decongestant, precursor for methamphetamine synthesis
Methylphenidate	Reuptake inhibitor (mainly dopamine)	ADHD, narcolepsy	Less euphoria than amphetamines, shorter duration of action
Atomoxetine	Norepinephrine reuptake inhibitor	ADHD	Non-stimulant alternative for ADHD

Abbreviations. ADHD: Attention-deficit hyperactivity disorder, CNS: Central nervous system, OTC: Over-the-counter, ↑: Increase, ↓: Decrease

ALERT: β-blockers should be avoided in patients with suspected cocaine intoxication as they can leave α1 effects unopposed, potentially worsening hypertension and causing coronary vasospasm.

NOTE: Cocaine causes mydriasis in eyes with intact sympathetic innervation, making it useful to confirm Horner syndrome diagnosis (lack of dilation indicates sympathetic denervation).

α2-Agonists (Sympatholytics)

Despite being agonists, these drugs reduce sympathetic output through central α2 receptor stimulation, reducing norepinephrine release and sympathetic outflow.

Table 3: Sympatholytics (α₂-Agonists): Applications and Adverse Effects

Drug	Applications	Adverse effects
Clonidine, Guanfacine	Hypertension, ADHD, Tourette syndrome, opioid withdrawal	CNS depression, bradycardia, hypotension, respiratory depression, rebound hypertension with abrupt cessation
α-Methyldopa	Hypertension in pregnancy	Direct Coombs ⊕ hemolysis, drug-induced lupus, hyperprolactinemia
Tizanidine	Muscle spasticity	Hypotension, weakness, dry mouth

Abbreviations. ADHD: Attention-deficit hyperactivity disorder, CNS: Central nervous system, ⊕: Positive (e.g., Coombs ⊕ = Coombs test positive)

Prototype Drugs and Their Hemodynamic Profiles

1. Norepinephrine (α > β)

● ↑↑ Mean arterial pressure (MAP)

● ↑ Systolic and diastolic BP

● Reflex bradycardia (baroreceptor response)

● Minimal ↑ in cardiac output

2. Epinephrine (β > α)

● ↑ Cardiac output

● ↑ Heart rate

● ↑ MAP (moderate)

● ↑ Pulse pressure

● Low dose: β effects predominate → possible ↓ diastolic BP

● High dose: α effects become significant → ↑ diastolic BP

3. Isoproterenol (β1 = β2)

● ↑↑ Heart rate

● ↑↑ Cardiac output

● ↓ Peripheral resistance (β2 effect)

● ↑ Pulse pressure

● MAP may remain unchanged or slightly ↑

Table 4: Comparing hemodynamic profiles of key sympathomimetics

Parameter	Norepinephrine	Epinephrine	Isoproterenol	Phenylephrine	Dobutamine
Heart Rate	↔/↓	↑	↑↑	↓	↑
Systolic BP	↑↑	↑	↑	↑↑	↔/↑
Diastolic BP	↑↑	↑/↓	↓↓	↑↑	↔/↓
Pulse Pressure	↔	↑	↑↑	↔	↑
Mean Arterial Pressure	↑↑	↑	↓	↑↑	↔
Cardiac Output	↔/↓	↑	↑↑	↓	↑↑
SVR	↑↑	↑/↓	↓↓	↑↑	↓
Predominant Effect	α₁ > β₁	β > α (dose-dependent)	β₁ = β₂	α₁	β₁ > β₂

Abbreviations. BP: Blood pressure, MAP: Mean arterial pressure, SVR: Systemic vascular resistance, ↔: No significant change, ↑ / ↓: Increase or decrease (variable effect depending on dose or reflex responses)

Adverse Effects

Table 5: Adverse effects of sympathomimetics by system

System	Adverse effects	Notes
Cardiovascular	Tachycardia, palpitations, hypertension, arrhythmias, myocardial ischemia, pulmonary edema (rare)	Risk increases in patients with pre-existing cardiovascular disease
Central Nervous System	Anxiety, restlessness, tremor, insomnia, headache, seizures (with overdose)	CNS effects more common with agents that cross blood-brain barrier
Metabolic	Hyperglycemia, hypokalemia, lactic acidosis	More pronounced with non-selective agents
Respiratory	Paradoxical bronchospasm (rare)	More common with non-selective agents
Genitourinary	Urinary retention, sexual dysfunction	Due to α₁-mediated effects
Ophthalmic	Mydriasis, increased intraocular pressure	Caution in patients with narrow-angle glaucoma
Gastrointestinal	Decreased motility, nausea	May worsen ileus
Peripheral	Vasoconstriction, tissue ischemia	With prolonged use of vasoconstrictors

Abbreviations. CNS: Central Nervous System, α₁: Alpha-1 adrenergic receptor, Non-selective agents: Drugs that stimulate multiple adrenergic receptor subtypes (e.g., β₁ and β₂ or α and β), Mydriasis: Pupil dilation, Ileus: Temporary paralysis of a portion of the intestine

References

Whalen, K. (2022). Lippincott illustrated reviews: Pharmacology (8th ed.). Wolters Kluwer.