adrenocorticotropic hormone(redirected from adrenocorticotropic)
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adrenocorticotropic hormone(ədrē`nōkôr'təkōtrŏp`ĭk), polypeptide hormone secreted by the anterior pituitary glandpituitary gland,
small oval endocrine gland that lies at the base of the brain. It is sometimes called the master gland of the body because all the other endocrine glands depend on its secretions for stimulation (see endocrine system).
..... Click the link for more information. . Its chief function is to stimulate the cortex of the adrenal glandadrenal gland
or suprarenal gland
, endocrine gland (see endocrine system) about 2 in. (5.1 cm) long situated atop each kidney. The outer yellowish layer (cortex) of the adrenal gland secretes about 30 steroid hormones, the most important of which are aldosterone and
..... Click the link for more information. to secrete adrenocortical steroids, chief among them cortisonecortisone
, steroid hormone whose main physiological effect is on carbohydrate metabolism. It is synthesized from cholesterol in the outer layer, or cortex, of the adrenal gland under the stimulation of adrenocorticotropic hormone (ACTH).
..... Click the link for more information. . The release of adrenocorticotropic hormone (ACTH), also known as corticotropin, is stimulated by corticotropin-releasing factor (CRF), a secretion of the hypothalamus. 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 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 is contingent upon normally functioning adrenal glands and is therefore useless in disorders caused by adrenal insufficiency, e.g., as replacement therapy where both adrenal glands have been removed.
(ACTH; also corticotropin), a hormone produced by the anterior lobe of the hypophysis. It stimulates the function of the cortex of the adrenal glands (the production of corticoids—in particular, hydrocortisone) and thereby contributes to the normal course of metabolic processes and to the increased resistance of human and animal organisms to the effects of unfavorable conditions.
ACTH is a peptide chain consisting of 39 amino acid residues and has a molecular weight of about 4,500. Its biological activity is due to the 24 amino acid residues that are closest to the amine end of the molecule, while the remaining 15 define the species characteristics and immunological properties of the hormone. In addition to its primary effects on the adrenal glands, ACTH also exhibits fat-mobilizing and melanocyte-stimulating activity. When the defense mechanisms of the body must be mobilized (during trauma, infection, stress situations, and so forth), increased amounts of ACTH are secreted into the blood.
The secretion of ACTH by the hypophysis is controlled by the hypothalamus. The regulatory influences from the hypothalamus are transmitted to the hypophysis by a neurohumoral substance, probably a peptide, found in the hypothalamus. This substance is called corticotropin releasing factor, or CRF.
ACTH is used as a hormonal preparation in the treatment of adrenocortical insufficiency caused by hypophyseal disorders, as well as in the treatment of rheumatism, polyarthritis, gout, bronchial asthma, eczema and other allergies, and other diseases. ACTH for medical use is obtained from the hypophyses of cattle. ACTH has also been synthesized; these preparations, which differ structurally from natural ACTH, have a higher biological activity.
REFERENCESPankov, Iu. A. “Khimiia AKTG i mekhanizm reguliatsii ego sekretsii.” Uspekhi sovremennoi biologii, 1959, vol. 47, no. 3.
Gorizontov, P. D., and T. N. Protasova. Rol’ AKTG i kortikos-teroidov v patologii. Moscow, 1968.
Schwyzer, R. “Chemistry and metabolic action of nonsteroid hormones.” Annual Review of Biochemistry, 1964, vol. 33, pp. 259–85.
IU. A. PANKOV