Autonomic pharmacology looks huge — dozens of drugs, dozens of effects. But it all collapses into one idea: know the transmitter and the receptor at each site, and every drug action follows. The map below is the framework the entire topic hangs on.
The two divisions
- Sympathetic (“fight or flight”) — thoracolumbar outflow; short pre-ganglionic, long post-ganglionic fibres.
- Parasympathetic (“rest and digest”) — craniosacral outflow; long pre-ganglionic, short post-ganglionic fibres.
The transmitter–receptor rules (memorise these)
- All pre-ganglionic fibres release ACh acting on nicotinic (NN) receptors in the ganglion.
- Parasympathetic post-ganglionic releases ACh on muscarinic receptors.
- Sympathetic post-ganglionic releases noradrenaline on adrenergic (α/β) receptors.
- Three exceptions worth marks: sympathetic fibres to sweat glands are cholinergic (muscarinic); the adrenal medulla is innervated by a pre-ganglionic fibre (ACh→N) and secretes adrenaline; the renal vascular bed uses dopamine.
Cholinergic receptors
- Nicotinic (N): ligand-gated ion channels — NM (neuromuscular junction) and NN (ganglia, CNS).
- Muscarinic (M1–M5): GPCRs — M1 (CNS, gastric glands), M2 (heart, slows it), M3 (smooth muscle, glands, eye).
Adrenergic receptors & their effects
- α1 — vasoconstriction, mydriasis, bladder sphincter contraction.
- α2 — pre-synaptic; inhibits noradrenaline release (clonidine lowers BP centrally).
- β1 — heart: ↑ rate, force, conduction; renin release.
- β2 — bronchodilation, vasodilation, uterine relaxation, glycogenolysis.
- β3 — lipolysis, bladder relaxation.
The drugs, by what they do
- Cholinergic agonists: pilocarpine (glaucoma), bethanechol (urinary retention).
- Anticholinesterases: neostigmine (myasthenia), physostigmine (crosses BBB), organophosphates (poisoning → treat with atropine + pralidoxime).
- Antimuscarinics: atropine, ipratropium, oxybutynin.
- Adrenergic agonists: adrenaline (anaphylaxis), noradrenaline (shock), phenylephrine (α1), salbutamol (β2, asthma), dobutamine (β1).
- Adrenergic antagonists: prazosin (α1), propranolol (non-selective β), atenolol/metoprolol (β1-selective).
Exam tip: don’t memorise effects — derive them. “Atropine blocks M” → no muscarinic action → tachycardia, dry mouth, mydriasis, urinary retention. Get the receptor right and the whole answer writes itself.
Master this single framework — transmitter, receptor, effector — and autonomic pharmacology stops being a list to cram and becomes a system you can reason through in the exam hall.
Test yourself
0 / 2A quick check on this topic — tap an answer for instant feedback.
Q1. Sympathetic post-ganglionic fibres to sweat glands release:
Sweat glands are the cholinergic (muscarinic) exception within the sympathetic system.Q2. β2 adrenergic receptors mediate:
β2 → bronchodilation and vasodilation; β1 acts on the heart; α1 causes vasoconstriction.
Question 1 of 2