Corticotrophin-releasing hormone CRH

The hypothalamus-pituitary system is of particular importance for steroid hormones. The formation of steroid hormones in the adrenal cortex is controlled by the pituitary hormone corticotrophin (ACTH), whose formation in turn is regulated by the corresponding releasing factor of the hypothalamus, corticotrophin releasing hormone (CRH). 

Corticotrophin releasing hormone (CRH), corti-coliberin, is a hypothalamic polypeptide that has diagnostic use. It increases ACTH secretion in Cushing s disease secondary to pituitary ACTH-secreting adenoma. It has no therapeutic use. 

Two neuropeptides, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) are released from parvoceUular neurons in the hypothalamic PVN to initiate a stress response. The terminal endings of these neurons, located in the median eminence of the hypothalamus, release CRH and AVP into the hypothalamic-hypophysial portal vessel system, where they travel to the anterior pituitary. The two neuropeptides act syn-ergistically on pituitary corticotrophs to activate the synthesis of pro-opiomelanocortin (POMC). This peptide, discussed in detail below, is processed to produce several peptides including adrenocorticotrophic hormone (ACTH), or corticotropin. ACTH released from corticotrophs travels via the bloodstream to act on cells in the zona fasciculata layer of the adrenal cortex, stimulating the synthesis and release of the glucocorticoids, cortisol (in humans) or corticosterone (in rodents). 

Corticotrophin-releasing hormone (CRH corticotrophin-releasing factor. CRF) controls release of corticotrophin (adrenocorticotrophic hormone. ACTH). which in turn controls the release of corticosteroids from the adrenal glands. See corticotrophin-releasing factor RECEPTOR agonists CORTICOTROPHIN-RELEASING FACTOR RECEPTOR ANTAGONISTS. 

Corticotrophin releasing hormone (CRH), a peptide synthesised in the paraventricular nucleus, suppresses appetite and food intake in addition to its role in the regulation of the hypothalamic-pituitary-adrenal axis. 

In addition to the alterations in gonadotrophic hormones described above, patients have an increased plasma cortisol, secondary to an elevation of corticotrophin releasing hormone (CRH) (Putignano et al. 2001). This is a factor in the reduction in bone density and increased liability to fractures seen in anorexia nervosa. Increased CRH inhibits the activity of the orexogenic neuropeptide Y (NPY) thereby further lowering the desire to eat. 

Cortisol is produced in the zona fasciculata and zona reticularis of the adrenal cortex, the end prixluct of a cascade of hormones which make up the hypothalamic-pituitary-adreniKortical axis (Fig. 2). Corticotrophin releasing hormone (CRH) is secreted by the hypothalamus under the influence of cerebral factors. Adrenocorticotrophic hormone (corticotrophin. orsimply ACTH) is secreted by the anterior pituitary under the control of CRH to maintain the fa.scicular and reticular zones of the adrenal cortex and to stimulate the secretion of cortisol. Ilypolhalamie secretion of CRH and pituitary secretion of ACTH are modulated by cortisol in negative feedback liwps. 

F. 43.7. Regulation of cortisol secretion. Various factors act on the hypothalamus to stimulate the release of corticotrophin-releasing hormone (CRH). CRH stimulates the release of ACTH from the anterior pituitary, which stimulates the release of cortisol from the adrenal cortex. Cortisol inhibits the release of CRH and ACTH. 

Disorders in sodium, potassium, and glucose may be noted owing to damage to the hypothalamus and pituitary that will affect the release of hormones that control metabolism (e.g., thyrotropin-releasing hormone [TRH] and thyroid-stimulating hormone [TSH]) and fluids and electrolytes (e.g., corticotrophin-releasing hormone [CRH] and adrenocorticotropin hormone [ACTH]). 

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