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The adrenal medulla and catecholamines !

  • Regulation
  • Exam priority: medium

The core of each adrenal gland is a nerve relay that pours adrenaline into the blood in seconds when the body faces danger or a drop in sugar.

Updated 2026-11-01

Also called: Chromaffin cells, Epinephrine, Adrenaline, Norepinephrine

See it in 3D: Left adrenal gland · Right adrenal gland · Sympathetic trunk

What it is

The adrenal medulla comes from neural crest and works as a modified sympathetic ganglion: preganglionic splanchnic fibres release acetylcholine onto chromaffin cells, which secrete catecholamines straight into the blood instead of onto a target organ. In humans about 80% of the output is epinephrine and about 20% norepinephrine. The response is fast (seconds) and short (half-life of about 2 minutes). Synthesis and breakdown chemistry is on the Biochemistry page.

How it works, step by step

  1. Stress, exercise, hypoglycemia or hypotension activate the hypothalamus and brainstem sympathetic centres.
  2. Preganglionic fibres in the splanchnic nerves release acetylcholine onto nicotinic receptors of chromaffin cells.
  3. Depolarization opens Ca²⁺ channels and the granules release catecholamines by exocytosis into the medullary veins.
  4. Epinephrine raises cardiac output (β1) and redistributes flow from skin and gut (α1) to muscle (β2).
  5. In the liver and muscle it activates glycogenolysis; in fat, lipolysis; in the pancreas it suppresses insulin (α2) and raises glucagon (β).
  6. COMT and MAO clear it within minutes, so the effect lasts only as long as the stimulus.

Adrenergic receptors and the effects of circulating catecholamines

ReceptorSecond messengerMain effectFavoured by
α1Gq: IP₃, Ca²⁺ ↑Vasoconstriction, mydriasisNE ≥ Epi
α2Gi: cAMP ↓Less insulin, less NE releaseNE ≈ Epi
β1Gs: cAMP ↑Heart rate, contractility, renin ↑NE = Epi
β2Gs: cAMP ↑Bronchodilation, muscle vasodilation, glycogenolysis, K⁺ into cellsEpi ≫ NE
β3Gs: cAMP ↑Lipolysis, bladder relaxationNE ≥ Epi

Clinical notes

  • Pheochromocytoma: episodic headache, sweating and palpitations with hypertension (sustained or paroxysmal); it may be part of MEN 2 or hereditary paraganglioma syndromes.
  • Blocking only β receptors in a catecholamine excess leaves α1 vasoconstriction unopposed and β2 vasodilation lost, so blood pressure can rise further.
  • Epinephrine pushes potassium into cells (β2): stress can lower serum K⁺ transiently.
  • Neuroblastoma, a childhood tumour of the same neural-crest lineage, also raises urinary catecholamine metabolites.

Test yourself

Think of the answer, then tap the question to see it.

Why do adrenal medullary cells make mostly epinephrine while sympathetic nerve endings make norepinephrine?

Only chromaffin cells bathed in cortical blood rich in cortisol express enough PNMT, which methylates norepinephrine to epinephrine.

Why does epinephrine lower diastolic pressure slightly at low concentrations but raise it at high ones?

At low levels it acts mainly on high-affinity β2 receptors, dilating muscle arterioles; at high levels α1 vasoconstriction dominates.

How does epinephrine raise blood glucose?

It drives hepatic glycogenolysis and gluconeogenesis, suppresses insulin through α2 receptors on beta cells, stimulates glucagon and reduces glucose uptake by muscle.

Why are plasma metanephrines a better screening test for pheochromocytoma than plasma catecholamines?

Tumours release catecholamines in bursts, but they convert them continuously to metanephrines inside the tumour (COMT), so metanephrines stay high between episodes.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

In Pharmacology

← All of physiology

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: 17.6 The Adrenal Glands (OpenStax (Rice University), 2022); Pheochromocytoma (StatPearls (NCBI Bookshelf), 2024); Catecholamine Tests: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 61). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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