Pharmacology · Topic 1 of 3
Autonomic pharmacology
30 min read
The autonomic nervous system is the backbone of pharmacology: a huge number of drugs, and their side effects, are explained by which autonomic receptors they stimulate or block. Learn the receptors and their effects first — the drugs then follow naturally.
The receptors
Every receptor has a G-protein and a set of target-organ effects worth knowing by heart.
- M2 (Gi) — slows the heart (SA and AV nodes)
- M3 (Gq) — bronchoconstriction, glandular secretion, miosis, bladder contraction
- α1 (Gq) — vasoconstriction, mydriasis, urinary sphincter contraction
- α2 (Gi) — reduces sympathetic outflow centrally
- β1 (Gs) — increases heart rate and contractility, renin release
- β2 (Gs) — bronchodilation, vasodilation in skeletal muscle, uterine relaxation
Cholinergic drugs
Direct agonists such as pilocarpine (glaucoma, dry mouth) stimulate muscarinic receptors. Acetylcholinesterase inhibitors — neostigmine, pyridostigmine, donepezil — increase acetylcholine at every cholinergic synapse.
Antimuscarinics such as atropine block M receptors: hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.
Adrenergic drugs
Adrenaline acts on α and β receptors and is the first-line drug for anaphylaxis (IM, 0.5 mg in adults). Salbutamol is a selective β2 agonist. Beta-blockers range from cardioselective (bisoprolol, metoprolol) to non-selective (propranolol) — the latter is contraindicated in asthma.
High-yield points
- Organophosphate poisoning = cholinergic excess (DUMBELS); treat with atropine + pralidoxime.
- Non-selective β-blockers can precipitate bronchospasm in asthma.
- Clonidine is a central α2 agonist; rebound hypertension occurs if stopped abruptly.
- Phenylephrine is a pure α1 agonist — it can cause reflex bradycardia.