Alternative names: Corticotrophin.
ACTH secretion is an excellent example of the regulation of a biological system by a negative-feedback mechanism; high levels of adrenocortical steroids in the blood tend to decrease ACTH release, whereas low steroid levels have the opposite effect.
ACTH secretion is increased when a person is in a stressful condition. ACTH is on the World Anti-Doping Agency's 2005 Prohibited List.
ACTH is available as a synthetic derivative in the form of cosyntropin (synthetic ACTH), trade name Cortrosyn®.
ACTH has the same pharmacologic and clinical effects as cortisone when given intravenously or intramuscularly; however, it has no value when applied externally and cannot be taken orally since it is deactivated by digestive enzymes. The action of ACTH depends upon normally functioning adrenal glands and ACTH is therefore useless in disorders caused by adrenal insufficiency, for example as replacement therapy where both adrenal glands have been removed.
ACTH acts through the stimulation of cell surface ACTH receptors, which are primarily located on the adrenocortical cells. ACTH stimulates the cortex of the adrenal gland and boosts the synthesis of corticosteroids, mainly glucocorticoids but also sex steroids (androgens).
One hormone which has been shown to shorten the duration and intensity of acute exacerbations is adrenocorticotropic hormone (ACTH), a pituitary gland substance that stimulates the adrenal glands to produce additional cortisone, which acts to reduce the inflammation in the brain or spinal cord. ACTH does not affect the underlying disease processes but may diminish the frequency and severity of exacerbations and even slow the progression of the disease.
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