Sympathomimetic Drugs: Adrenergic Pharmacology and Clinical Applications

3rd Year MBBS • Infection and Inflammation

Connect receptor selectivity, organ effects, clinical uses, toxicity and important drug interactions for rapid revision.

1. THE TOPIC IN ONE CONNECTED FLOW

Sympathomimetics increase adrenergic activity either by directly stimulating adrenoceptors or by increasing endogenous catecholamine availability. Their clinical effects can be predicted from the receptor involved: α receptors mainly influence vascular tone, β receptors mainly affect the heart and smooth muscle, while dopamine shows dose-dependent receptor effects.

Sympathomimetic Drug

Direct acting or increased endogenous catecholamine activity

→

Receptor Activation

α₁ • α₂ • β₁ • β₂ • D₁

→

Organ Effect

Vascular tone, cardiac activity, bronchial tone or aqueous humour changes

→

Therapeutic Effect

Blood-pressure support, bronchodilation, anaphylaxis treatment or reduced intraocular pressure

→

Excess Adrenergic Effect

Hypertension, palpitations, tremor or arrhythmias

→

Important Interaction

MAO inhibition + tyramine or indirect sympathomimetic → excessive noradrenaline → severe hypertension

2. KEY CLINICAL CONNECTIONS

Anaphylaxis

Adrenaline
→
α₁ vasoconstriction
→
improved blood pressure and reduced mucosal edema

β₂ stimulation
→
bronchodilation
→
improved airflow

Cardiovascular Drug Comparison

Noradrenaline
→
strong α-mediated vasoconstriction
→
raised systolic and diastolic pressure
→
reflex bradycardia

Isoprenaline
→
β₁ + β₂ stimulation
→
tachycardia with reduced diastolic pressure

Glaucoma

Brimonidine
→
α₂ stimulation
→
reduced aqueous humour formation

Acetazolamide
→
carbonic anhydrase inhibition
→
reduced aqueous production

Mannitol
→
increased plasma osmolarity
→
water leaves ocular tissues
→
rapid pressure reduction

3. AIM HIGH-YIELD INTEGRATION REVIEW

⭐ α₁ stimulation
→
vascular smooth-muscle contraction
→
increased peripheral resistance and blood pressure.

β₁ stimulation
→
increased heart rate and contractility
→
increased cardiac output.

⭐ β₂ stimulation
→
bronchial smooth-muscle relaxation
→
bronchodilation.

Noradrenaline
→
major rise in arterial pressure
→
baroreceptor activation
→
reflex bradycardia.

⭐ Dopamine dose rises
→
D₁
→
β₁
→
α₁ predominance
→
vasodilation, then cardiac stimulation, then vasoconstriction.

Catecholamine structure
→
rapid COMT and MAO metabolism
→
short duration and poor oral effectiveness.

⭐ MAO inhibition + tyramine
→
excessive noradrenaline release
→
severe hypertension.

Adrenaline overdose
→
excessive α-mediated vasoconstriction
→
severe hypertension
→
α-adrenoceptor blockade with phentolamine may directly oppose the vascular effect.

AIM Exam Trap:
Noradrenaline directly stimulates β₁ receptors, yet the pulse may fall because its strong α-mediated rise in blood pressure triggers reflex bradycardia. Isoprenaline produces the opposite pattern: β₁ stimulation increases heart rate while β₂ vasodilation lowers peripheral resistance.