Corticotrophin-releasing hormone , secretion

In six hypertensive patients given nitrendipine 20 mg/day for 30 days, there was inhibition of aldosterone response but no significant change in ACTH secretion in response to corticotrophin-releasing hormone (225). 

There is a major negative feedback loop involving the hypothalamus, corticotrophin-releasing hormone, corticotropin (=ACTH) secreted by the pituitary and corticosteroids from the adrenal cortex, which dampen pro-inflammatory cytokine production. This loop normally acts to stabilise immune system activity, but it also has spillover effects on appetite and weight regulation. 

The paraventricular nucleus of the hypothalamus releases corticotrophin-releasing hormone, which stimulates the pituitary gland to release adrenocorticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated levels of cortisol exert negative feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. 

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. 

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. 

The class III cytokine receptor family includes two TNE receptors, the low affinity NGE receptor and 7-ceU surface recognition sites that appear to play a role in proliferation, apoptosis, and immunodeficiency. TNE-a (- 17, 000 protein) is produced by astrocytes and microglia and can induce fever, induce slow-wave sleep, reduce feeding, stimulate prostaglandin synthesis, stimulate corticotrophin-releasing factor and prolactin secretion, and reduce thyroid hormone secretion. TNE-a stimulates IL-1 release, is cytotoxic to oligodendrocytes, and reduces myelination this has been impHcated in multiple sclerosis and encephalomyelitis. Astrocyte TNE-a receptors mediate effects on IL-6 expression and augment astrocytic expression of MHC in response to other stimulants such as lEN-y. 

Corticotropin (corticotrophin adrenocorticotrophin ACTH) is a straight-chain polypeptide with39 amino acid residues, and its function is to control the activity of the adrenal cortex, particularly the production of corticosteroids. Secretion of the hormone is controlled by corticotropin-releasing hormone (CRH) from the hypothalamus. ACTH was formerly used as an alternative to corticosteroid therapy in rheumatoid arthritis, but its value was limited by variable therapeutic response. ACTH may be used to test adrenocortical function. It has mainly been replaced for this purpose by the synthetic analoguetetracosactide (tetracosactrin) (Figure 7.10), which contains the first 24 amino acid residues of ACTH, and is preferred because of its shorter duration of action and lower allergenicity. 

Figure 18.4. Endocrine-immune inter-relationship following acute stress. In response to stress, corticotrophin releasing factor (CRF) and arginine vasopressin (AVP) are secreted from the hypothalamus causing the release of adrenocortico-trophic hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol on the hypothalamus, pituitary and immune system remains unaffected in acute stress - the release of CRF, AVP and immunotransmitters is still inhibited, preventing the continual activation of the...

Q4 Glucocorticoid secretion is controlled by the hypothalamus and anterior pituitary gland. Corticotrophin releasing factor (CRF) is produced in the hypothalamus and travels in the hypophyseal portal blood vessels to the anterior pituitary to release ACTH (adrenocorticotrophic hormone). There is a daily (circadian) rhythm in CRF and ACTH secretion, with a peak in the morning between 7 and 9 a.m. and a low point during the night. 

Corlan hydrocortisone, corticoliberin corticotrophin-releasing factor, corticorelin corticotrophin-releasing factor. CORTICOSTEROIDS as a family are natural steroid hormones secreted by the adrenal cortex, or are synthetic substances that closely resemble them. There are two main types GLUCOCORTICOIDS (corticosterone. cortisone and hydrocortisone) are essential for utilization of carbohydrate, fat and protein in the body, and in the normal response to stress. Naturally occurring and synthetic glucocorticoids have a powerful antiinflammatory effect. 

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