Autonomic Pharmacology Basics
Direct answer
Autonomic pharmacology covers drugs that mimic or block the sympathetic and parasympathetic nervous systems. The sympathetic outflow is thoracolumbar (T1–L2/3) with short preganglionic and long postganglionic fibres; the parasympathetic is craniosacral (nerves III, VII, IX, X and S2–S4) with long preganglionic and short postganglionic fibres. All preganglionic fibres release acetylcholine on nicotinic ganglionic (Nn) receptors; postganglionic parasympathetic fibres release acetylcholine on muscarinic receptors, and sympathetic postganglionic fibres release noradrenaline on alpha and beta receptors — the sweat glands being the classic cholinergic exception.
What you must remember
- The cholinergic exception: sympathetic fibres to sweat glands release acetylcholine on muscarinic receptors; the adrenal medulla is a modified sympathetic ganglion releasing mainly adrenaline (about 80 per cent) on nicotinic stimulation.
- Alpha receptors: alpha-1 (Gq) causes vasoconstriction, mydriasis and contraction of prostate and bladder neck — blockers such as tamsulosin relieve prostatic obstruction but cause orthostatic hypotension; alpha-2 (Gi) presynaptically inhibits noradrenaline release, the basis of clonidine.
- Beta receptors: beta-1 (Gs) increases heart rate, contractility and renin release — blocked by atenolol and metoprolol; beta-2 causes bronchodilation, uterine relaxation and skeletal muscle vasodilation — activated by salbutamol; beta-3 mediates detrusor relaxation and lipolysis.
- Cholinergic receptors: M2 in the heart producing bradycardia; M3 on glands and smooth muscle producing bronchoconstriction, increased gastrointestinal motility, detrusor contraction and miosis; nicotinic Nm at the neuromuscular junction (blocked by vecuronium, depolarised by succinylcholine) and Nn at ganglia.
- Atropine, the prototype antimuscarinic: dry mouth, mydriasis with cycloplegia, tachycardia, urinary retention, constipation, cutaneous vasodilatation with hyperthermia; used preanaesthetically, in organophosphate poisoning, and before neostigmine when reversing neuromuscular block.
- Neostigmine, a cholinesterase inhibitor, raises acetylcholine everywhere: used in myasthenia gravis, postoperative ileus and reversal of competitive block.
- Adrenaline is the drug of choice in anaphylaxis (intramuscular): alpha-1 raises blood pressure, beta-2 relieves bronchospasm and limits mast cell mediator release; noradrenaline is predominantly an alpha-1 vasoconstrictor; dopamine acts on D1, beta-1 and alpha-1 receptors dose-dependently.
Common confusion
Students assume every sympathetic postganglionic fibre is adrenergic — forgetting sweat glands — and call noradrenaline a beta-2 agonist, whereas it raises pressure purely by alpha-1 vasoconstriction with reflex bradycardia, while adrenaline's beta-2 effect lowers diastolic pressure. Remember also that only cranial nerves III, VII, IX and X carry parasympathetic fibres.
Exam-focused takeaway
In theory, draw one autonomic synapse with its receptor sites — preganglionic Nn, postganglionic alpha, beta or muscarinic — and place drug examples on the diagram. In viva, expect organ-level questions: atropine on pupil, heart and bowel, drugs avoided in asthma, adrenaline's route in anaphylaxis. In practicals, justify autonomic drug choices such as a beta-2 agonist in asthma and write the prescription in full.
Practise MCQs and previous-year questions on autonomic pharmacology in the PrepElephant app. Free notes continue on this website.
Frequently asked questions
Which sympathetic fibres release acetylcholine?
Preganglionic fibres, fibres to eccrine sweat glands and some vessels, and the fibres to the adrenal medulla; all other postganglionic sympathetic fibres release noradrenaline.
Why is atropine given with neostigmine?
Neostigmine raises acetylcholine at nicotinic sites (desired) and muscarinic sites (undesired); atropine or glycopyrrolate blocks the bradycardia, secretions and bronchospasm.
Why are non-selective beta-blockers avoided in asthma?
Propranolol blocks bronchial beta-2 receptors and can precipitate severe bronchospasm; cardioselective beta-1 blockers are preferred if one is essential.
What is the cheese reaction?
Patients on monoamine oxidase inhibitors cannot metabolise dietary tyramine, which releases stored catecholamines and causes hypertensive crisis after tyramine-rich foods such as cheese.
Why is adrenaline preferred over noradrenaline in anaphylaxis?
Anaphylaxis needs alpha-1 pressure support plus beta-2 bronchodilation and mast cell stabilisation; noradrenaline offers only vasoconstriction.
Practise this in the PrepElephant app
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