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Adrenergic and cholinergic receptors !

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Adrenaline and acetylcholine act through different receptor types; knowing which type sits on an organ predicts what a drug will do.

Updated 2026-11-01

Also called: Alpha and beta receptors, Muscarinic and nicotinic receptors

See it in 3D: Sinoatrial (SA) node · Main bronchi

What it is

Adrenergic receptors (α1, α2, β1, β2, β3) respond to norepinephrine and epinephrine. Cholinergic receptors are nicotinic (ion channels in ganglia, adrenal medulla and skeletal muscle) or muscarinic (M1–M5, G protein receptors on parasympathetic targets). Each G protein receptor uses a second messenger: Gq raises IP₃ and Ca²⁺, Gs raises cAMP and Gi lowers it. The receptor on each organ predicts what a drug or a toxin will do there.

Receptors, messengers and effects

ReceptorG protein / messengerMain sitesEffect
α1Gq: IP₃, DAG, Ca²⁺ ↑Vascular smooth muscle, iris dilator, internal urethral sphincterVasoconstriction, mydriasis, urinary retention
α2Gi: cAMP ↓Presynaptic terminals, brainstem, pancreatic β cellsLess norepinephrine release, less insulin
β1Gs: cAMP ↑Heart, juxtaglomerular cells↑ rate, contractility and conduction; renin release
β2Gs: cAMP ↑Bronchi, skeletal muscle arterioles, uterus, liverBronchodilation, vasodilation, uterine relaxation, glycogenolysis
β3Gs: cAMP ↑Adipose tissue, bladder detrusorLipolysis, detrusor relaxation
M2Gi: cAMP ↓, K⁺ channels openSA and AV nodes, atria↓ heart rate and AV conduction
M3Gq: IP₃, Ca²⁺ ↑Bronchi, gut, detrusor, glands, endothelium, pupil sphincterContraction, secretion, miosis, NO-mediated vasodilation
Nicotinic (NN, NM)Ligand-gated cation channelAutonomic ganglia, adrenal medulla; skeletal muscle endplateFast depolarization

Clinical notes

  • Nonselective β-blockers can trigger bronchospasm in asthma (β2 blockade) and hide the tremor and tachycardia that warn of hypoglycemia.
  • Anticholinergic toxicity: hot dry skin, flushing, dilated pupils, urinary retention, ileus, delirium.
  • Organophosphate insecticide poisoning, a real risk in rural Colombia, blocks acetylcholinesterase: salivation, bronchorrhea, miosis and bradycardia, then fasciculations and weakness.
  • In anaphylaxis epinephrine acts on α1 (vasoconstriction) and β2 (bronchodilation, less mediator release from mast cells).

Test yourself

Think of the answer, then tap the question to see it.

Why can a nonselective β-blocker worsen asthma while metoprolol does so less?

Airway relaxation depends on β2 receptors raising cAMP. Nonselective drugs block β2; metoprolol is relatively β1-selective, although selectivity fades at high concentrations.

What explains the pupils and the heart rate in organophosphate poisoning?

ACh builds up: M3 on the pupil sphincter causes miosis and M2 on the SA node causes bradycardia. Nicotinic stimulation of ganglia can sometimes give tachycardia instead.

Why does stimulating α2 receptors in the brainstem lower blood pressure?

α2 receptors are Gi-coupled: they reduce norepinephrine release and sympathetic outflow from the vasomotor centre, so vascular tone and heart rate fall.

Why does a β2 agonist lower plasma potassium?

β2 stimulation raises cAMP and activates the Na⁺/K⁺-ATPase, mainly in skeletal muscle, shifting K⁺ from plasma into cells.

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The structures of Durgical's 3D anatomy where it happens.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 15.1 Divisions of the Autonomic Nervous System (OpenStax (Rice University), 2022); 15.4 Drugs that Affect the Autonomic System (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 61). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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