Autonomic Physiology
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Direct answer
Two neurons carry every autonomic command: a myelinated preganglionic fibre releasing acetylcholine onto nicotinic receptors, and a postganglionic fibre delivering the effector signal — acetylcholine again at muscarinic receptors in the parasympathetic arm and at sympathetic sweat glands, noradrenaline everywhere else in the sympathetic arm. The sympathetic outflow is thoracolumbar (T1 to L2-L3) with short preganglionic fibres ending in the paravertebral chain of about 22 ganglia or the prevertebral plexuses; the parasympathetic outflow is craniosacral — cranial nerves III, VII, IX and X, plus S2-S4 — with long preganglionic fibres synapsing on or near the target organ. The adrenal medulla is a modified sympathetic ganglion flooded by preganglionic acetylcholine, releasing about 80 per cent adrenaline and 20 per cent noradrenaline. Adrenergic receptors follow a functional alphabet: alpha-1 constricts vessels and dilates pupils, alpha-2 brakes transmitter release, beta-1 drives the heart, beta-2 dilates bronchi and skeletal muscle vessels, and D1 dopamine receptors dilate renal and mesenteric beds.
What you must remember
- Anatomical rule: sympathetic thoracolumbar T1-L2/L3, short pre- and long postganglionic fibres; parasympathetic craniosacral (III, VII, IX, X, S2-S4), long pre- and very short postganglionic fibres; the vagus carries about 75 per cent of all parasympathetic fibres.
- Neurotransmitter rule: all preganglionic fibres and all parasympathetic postganglionic fibres are cholinergic; sympathetic postganglionic fibres are noradrenergic except to sweat glands (cholinergic-muscarinic) and some muscle vessels (cholinergic for vasodilatation).
- Adrenal medulla: chromaffin cells are modified postganglionic neurons innervated by preganglionic cholinergic fibres; secretion roughly 80 per cent adrenaline, 20 per cent noradrenaline, with PNMT induced by cortisol.
- Receptor map: alpha-1 (Gq) vasoconstriction, mydriasis, sphincter contraction; alpha-2 (Gi) presynaptic inhibition; beta-1 (Gs) chronotropy and inotropy; beta-2 bronchodilatation, vasodilatation, uterine relaxation; M1-M3 muscarinic glands, smooth muscle, heart (M2 slows).
- Eye: parasympathetic (Edinger-Westphal, III) constricts the pupil and accommodates; sympathetic dilates (radial muscle) and raises the lid — Horner syndrome (ptosis, miosis, anhidrosis, apparent enophthalmos) follows sympathetic interruption anywhere along the chain.
- Organs without parasympathetic supply: most blood vessels, sweat glands, piloerector muscles and the adrenal medulla receive only sympathetic fibres.
- Pelvic physiology: parasympathetic sacral outflow drives erection (NO-mediated), bladder detrusor contraction and bowel motility; sympathetic drives ejaculation and internal sphincter tone — the classic autonomic casualty of diabetic neuropathy.
One drug, traced through the two arms
Atropine shows how the two arms differ. Block every muscarinic receptor and the parasympathetic arm collapses: pupils dilate, accommodation paralyses, salivation and sweating stop, the heart speeds (vagal withdrawal, the tachycardia of 100-plus in anaesthesia), gut motility falls and urine retention threatens. The sympathetic arm, though, barely notices — its ganglia use nicotinic receptors, and its postganglionic noradrenaline acts on adrenergic receptors. Now reverse the thought with a ganglion blocker such as hexamethonium: both arms fail together, because both share the same nicotinic synapse — and the body's baseline reveals itself as sympathetically driven vascular tone, since blood pressure falls profoundly. Finally give a beta-blocker before atropine in a heart-rate question: the tachycardia expected from vagal blockade is blunted, proving the heart's rate is set by the algebra of both arms, vagal restraint minus sympathetic drive, rather than by either alone. These three manipulations are exactly how the screening exam phrases its autonomic options.
Where students slip
First slip: "all postganglionic sympathetic fibres release noradrenaline" — sweat glands are the exception the exam hunts for, cholinergic-muscarinic, which is why they keep sweating in Horner syndrome only if the lesion is below the sweat fibre's divergence point, and why atropine (not a beta-blocker) causes anhidrosis. Second, receptor-location logic: alpha-2 agonists like clonidine lower blood pressure precisely because the dominant alpha-2 population is presynaptic — reducing release — not vasoconstrictive. Third, the pupillary exam: a dilated pupil from third-nerve palsy presents with ptosis and impaired eye movements, while pharmacological or sympathetic mydriasis keeps the lid and movements intact; the eye is the exam's favourite autonomic end-organ because one millimetre of pupil encodes the whole system.
Frequently asked questions
Which fibres of the autonomic nervous system are cholinergic?
All preganglionic fibres (sympathetic and parasympathetic), all parasympathetic postganglionic fibres, and the sympathetic postganglionic fibres to sweat glands.
What is the ratio of adrenaline to noradrenaline secreted by the adrenal medulla?
Roughly 80 per cent adrenaline to 20 per cent noradrenaline, released by chromaffin cells driven directly by preganglionic cholinergic fibres.
Which organs receive only sympathetic innervation?
Most blood vessels, sweat glands, piloerector muscles and the adrenal medulla have no parasympathetic supply.
Why does blocking the vagus speed the heart?
Vagal muscarinic (M2) action on the sinoatrial node is the dominant resting brake; removing it, as with atropine, unveils sympathetic tone and heart rates above 100.
What are the components of Horner syndrome?
Ptosis, miosis and anhidrosis with apparent enophthalmos, from interruption of the sympathetic pathway — preganglionic causes include apical lung tumours and stellate ganglion lesions.