Autonomic tone and denervation supersensitivity
- Regulation
- For completeness
Autonomic nerves fire slowly all the time; that steady tone lets them turn organs up or down, and cutting them makes organs oversensitive.
Also called: Sympathetic tone, Parasympathetic tone, Pharmacological pupil testing
See it in 3D: Sympathetic trunk · Vagus nerve
What it is
Autonomic effectors respond fully at low firing rates, and the nerves discharge continuously at a basal rate called tone. Tone lets one division both increase and decrease an organ's activity, for example vessel diameter. When a nerve is cut, tone is lost at once; within days to weeks the organ becomes more sensitive to its transmitter (denervation supersensitivity), which is the basis of several pupil tests.
How it works, step by step
- Autonomic nerves fire continuously at a low rate set by brainstem and hypothalamic centers.
- Because effectors respond to small changes in rate, centers can raise or lower activity smoothly from this baseline.
- Cutting the nerve removes tone at once, so the organ shifts toward the opposite state (vessels dilate, heart rate rises after vagotomy).
- Over days the denervated cells increase receptor number and lose the transmitter-clearing terminal.
- Tiny amounts of circulating or applied agonist then produce a large response: supersensitivity.
Regulation
- +Sympathetic tone (vessels): Keeps arterioles partly constricted; its loss drops peripheral resistance.
- −Vagal tone (heart): Holds resting heart rate well below the intrinsic SA node rate of about 100/min.
- +Adrenal medulla basal secretion: Adds circulating epinephrine and norepinephrine that support tone even when nerves are quiet.
- +Denervation (after days to weeks): More receptors and, for postganglionic loss, no reuptake: exaggerated response to transmitter or agonists.
Clinical notes
- Hypotension after high spinal anesthesia or cervical cord injury reflects sudden loss of sympathetic vascular tone.
- In Horner syndrome, the cocaine test shows failure of the affected pupil to dilate, since there is no norepinephrine release to prolong; apraclonidine dilates it through supersensitivity.
Test yourself
Think of the answer, then tap the question to see it.
Why does a Horner pupil dilate with apraclonidine while a normal pupil hardly changes?
The denervated iris dilator has up-regulated α1 receptors, so apraclonidine's weak α1 action becomes strong (denervation supersensitivity).
How can the sympathetic system dilate a blood vessel without any vasodilator nerve?
By lowering its tonic firing below the resting rate, which reduces constriction.
Why does resting heart rate rise after both vagi are blocked?
Resting vagal tone normally slows the SA node below its intrinsic rate; removing it lets the node fire near 100/min.
Connections
See it in 3D2
The structures of Durgical's 3D anatomy where it happens.
In Pharmacology2
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: Horner syndrome: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Neuroanatomy, Cranial Nerve 10 (Vagus Nerve) (StatPearls (NCBI Bookshelf), 2025); Spinal Cord Injuries (StatPearls (NCBI Bookshelf), 2025).
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Representative model, for educational purposes only.