Adrenocorticotropic hormone

Adrenocorticotropic hormone (ACTH) is made in the pituitary gland. It is needed for your adrenal glands to work properly and help your body react to stress. ACTH stimulates the release of another hormone called cortisol from the cortex (outer part) of the adrenal gland.

Alternative names for adrenocorticotropic hormone

ACTH; adrenocorticotrophin; corticotropin

What is adrenocorticotropic hormone? 

Corticotrophin-releasing hormone from the <a href='/glands/hypothalamus/'>hypothalamus</a> acts on the pituitary (inset), which secretes ACTH. ACTH travels to the <a href='/glands/adrenal-glands/'>adrenal glands</a> via the bloodstream (arrow). <a href='/hormones/Cortisol/'>Cortisol</a> from the adrenal then feeds back to the hypothalamus to shut down the cycle.

Corticotrophin-releasing hormone from the hypothalamus acts on the pituitary (inset), which secretes ACTH. ACTH travels to the adrenal glands via the bloodstream (arrow). Cortisol from the adrenal then feeds back to the hypothalamus to shut down the cycle.

ACTH is made in the corticotroph cells of the anterior pituitary gland, where it is released in bursts into the bloodstream and transported around the body. Like cortisol, levels of adrenocorticotropic hormone are generally high in the morning when we wake up and fall throughout the day (reaching their lowest level during sleep). This is called a diurnal (circadian) rhythm. Once adrenocorticotropic hormone reaches the adrenal glands, it binds on to receptors causing the adrenal glands to secrete more cortisol, resulting in higher levels of cortisol in the blood. It also increases production of the chemical compounds that trigger an increase in other hormones such as adrenaline and noradrenaline.

How is adrenocorticotropic hormone controlled?

Secretion of ACTH is controlled by three regions of the body, the hypothalamus, the pituitary gland and the adrenal glands. This is called the hypothalamic–pituitary–adrenal (HPA) axis. When adrenocorticotropic hormone levels in the blood are low, a group of cells in the hypothalamus release a hormone called corticotrophin-releasing hormone which stimulates the pituitary gland to secrete ACTH into the bloodstream. High levels of ACTH are detected by the adrenal gland receptors which stimulate the secretion of cortisol, causing blood levels of cortisol to rise. As the cortisol levels rise, they start to slow down the release of corticotrophin-releasing hormone from the hypothalamus  (long loop inhibition) and ACTH (short loop inhibition) from the pituitary gland. As a result, the ACTH levels start to fall. This is called a negative feedback loop.

Stress, both physical and psychological, also stimulates ACTH production and hence increases cortisol levels.

What happens if I have too much adrenocorticotropic hormone?

The effects of too much ACTH are mainly due to the increase in cortisol levels. Higher than normal levels of adrenocorticotropic hormone may be due to:

  • Cushing's disease – this is the most common cause of increased ACTH. It is caused by a non-cancerous tumour called an adenoma located in the pituitary gland, which produces excess amounts of ACTH. (Please note, Cushing’s disease is just one of the numerous causes of Cushing’s syndrome).
     
  • A tumour, outside the pituitary gland, producing ACTH (also called ectopic ACTH tumour).
     
  • Adrenal insufficiency including Addison's disease (although cortisol levels are low, ACTH levels are raised).
     
  • Congenital adrenal hyperplasia (a genetic disorder with inadequate production of cortisol, aldosterone or both).

Other chemical compounds secreted with ACTH can also lead to hyper-pigmentation.

What happens if I have too little adrenocorticotropic hormone?

Lower than normal levels of adrenocorticotropic hormone may be due to:

  • Cushing's syndrome related to an adrenal tumour.
     
  • Cushing's syndrome due to steroid medication.
     
  • Conditions affecting the pituitary gland, e.g. hypopituitarism.
     
  • Side-effect of pituitary surgery or radiation therapy.

 


Last reviewed: Feb 2017