CorpusHuman Anatomy
EndocrineHormone

Corticotropin-releasing hormone (CRH)

Also known as: CRH, CRF, corticoliberin

A 41-amino-acid peptide from paraventricular neurons that drives ACTH release and orchestrates the endocrine, autonomic and behavioural responses to stress.

Show on body map Hypothalamic–Pituitary Axis

Overview

ClassPeptide (41 amino acids)
ReceptorCRHR1 — Gs, cAMP
SourceParaventricular nucleus
TargetCorticotrophs

CRH is secreted into the portal blood in a circadian pattern (highest in the early morning) and in bursts with any physical or psychological stressor. At corticotrophs it binds CRH receptor 1 (CRHR1), a Gs-coupled GPCR; cAMP/PKA stimulates both ACTH release and transcription of the POMC gene. Parvocellular neurons co-release ADH, which acts on V1b (V3) receptors on corticotrophs and synergistically amplifies CRH — especially in chronic stress.

Within the brain, CRH acts as a neurotransmitter that activates the locus coeruleus and sympathetic outflow and produces anxiety-like behaviour and suppression of appetite and reproduction. The placenta also produces large amounts of CRH in late pregnancy; rising placental CRH (the "placental clock") is linked to the timing of parturition.

Location

Source: parvocellular paraventricular neurons → median eminence (also placenta, limbic system). Target: corticotrophs of the anterior pituitary.

Function

  • Stimulates ACTH (and other POMC peptides) secretion.
  • Coordinates central stress responses (arousal, sympathetic activation).
  • Inhibits GnRH secretion (stress-related amenorrhoea).
Physiology

Class: 41-amino-acid peptide. Receptor: CRHR1 (Gs → cAMP); CRHR2 elsewhere. Plasma CRH-binding protein buffers placental CRH in pregnancy.

Regulation

Stimulated by stress (pain, hypoglycaemia, hypotension, infection via IL-1/IL-6, fear) and the suprachiasmatic clock; inhibited by cortisol (negative feedback at hypothalamus and pituitary).

Clinical significance

Hypercortisolism and HPA suppression

Long-term exogenous glucocorticoids suppress CRH and ACTH, causing adrenal atrophy; abrupt withdrawal precipitates secondary adrenal insufficiency, so long courses are tapered.

CRH test

Exogenous CRH increases ACTH and cortisol in pituitary Cushing disease but not in ectopic ACTH secretion; it is used during inferior petrosal sinus sampling.

Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.