Adrenocorticotropic hormone secretion

Pharmacotherapy generally is reserved for patients (1) in whom the ectopic adrenocorticotropic hormone-secreting tumor cannot be localized (2) who are not surgical candidates (3) who have failed surgery (4) who have had a relapse after surgery or (5) in whom adjunctive therapy is required to achieve complete remission. 

Wotjak CT, Kubota M, Liebsch G, Montkowski A, Holsboer F, Neumann I, Landgraf R (1996) Release of vasopressin within the rat paraventricular nucleus in response to emotional stress a novel mechanism of regulating adrenocorticotropic hormone secretion J Neu-rosci 16 7725-7732... 

Pregnenolone is transported from the mitochondria to the ER, where a hydroxyl oxidation and migration of the double bond yield progesterone. Pregnenolone synthesis in the adrenal cortex is activated by adrenocorticotropic hormone (ACTH), a peptide of 39 amino acid residues secreted by the anterior pituitary gland. 

Adrenal hormone production is controlled by the hypothalamus and pituitary gland. Corticotropin-releasing hormone (CRH) is secreted by the hypothalamus and stimulates secretion of adrenocorticotropic hormone (ACTH), also known as corticotropin from the anterior pituitary. ACTH, in turn, stimulates the adrenal cortex to produce cortisol. When sufficient or excessive cortisol levels are reached, a negative feedback is exerted on the secretion of CRH and ACTH, thereby decreasing overall cortisol production. The control of adrenal androgen synthesis also follows a similar negative-feedback mechanism. 

Adrenocorticotropic hormone A hormone secreted by the anterior pituitary that controls secretion of cortisol from the adrenal glands also referred to as corticotropin. 

A trophic hormone acts on another endocrine gland to stimulate secretion of its hormone. For example, thyrotropin, or thyroid-stimulating hormone (TSH), stimulates the secretion of thyroid hormones. Adrenocorticotropin, or adrenocorticotropic hormone (ACTH), stimulates the adrenal cortex to secrete the hormone cortisol. Both trophic hormones are produced by the pituitary gland in fact, many trophic hormones are secreted by the pituitary. The pituitary gland is sometimes referred to as the "master gland" because its hormones regulate the activity of other endocrine glands. 

Nickel ions have been shown to depress the in vivo and in vitro release of prolactin [336], while the release of growth hormone was stimulated, and only at relatively high ion concentrations. Hyperglycemia occurs in rats following intraperitoneal or intratracheal injections of NiCl2 [265, 337, 338], The mechanism of action of nickel appears to be inhibition of insulin release this inhibition could be related to the extremely high concentration of nickel found in the pituitary and the effect on the secretion of the pituitary hormones (growth hormone and adrenocorticotropic hormone). 

As would be expected of active protein secreting cells, glandular epithelial tissue, the cytokine secreting cells of the immune system and the blood vessel endothelium, have an extensive internal structure consisting of rough endoplasmic reticulum and numerous mitochondria. Peptide hormones, growth factors and cytokines like all proteins are synthesized by DNA transcription and mRNA translation. The primary transcript of the mRNA may code for an inactive prohormone which requires careful proteolysis to produce the active hormone, as for example in the case of insulin. Adrenocorticotropic hormone (ACTH) is particularly interesting in this respect because... 

See Table 15-6. Potassium-sparing diuretics are most useful in states of mineralocorticoid excess or hyperaldosteronism (also called aldosteronism), due either to primary hypersecretion (Conn s syndrome, ectopic adrenocorticotropic hormone production) or secondary hyperaldosteronism (evoked by heart failure, hepatic cirrhosis, nephrotic syndrome, or other conditions associated with diminished effective intravascular volume). Use of diuretics such as thiazides or loop agents can cause or exacerbate volume contraction and may cause secondary hyperaldosteronism. In the setting of enhanced mineralocorticoid secretion and excessive delivery of Na+ to distal nephron sites, renal K+ wasting occurs. Potassium-sparing diuretics of either type may be used in this setting to blunt the K+ secretory response. 

In addition to its central effects on blood pressure, Ang II acts on the central nervous system to stimulate drinking (dipsogenic effect) and increase the secretion of vasopressin and adrenocorticotropic hormone (ACTH). The physiologic significance of the effects of Ang II on drinking and pituitary hormone secretion is not known. 

The adenohypophysis is the part of the gland in which the tropic hormones are secreted They include the adrenocorticotropic hormone lACTHl. die thyrotropic hormone (TSH). and. somatotropin, as well as three hormones with pronounced effects upon the gonads the hormone prolactin, the follicle-stimulating hormone tFSHl and the luteinizing or interstitial cell stimulating hormone tLH or ISCH)... 

Anterior Lobe. The anterior pituitary, or adenohypophysis, secretes six important peptide hormones. The anterior pituitary releases growth hormone (GH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), and prolactin (Pr). The physiologic effects of these hormones are listed in Table 28-1. 

The primary glucocorticoid released in humans is cortisol (also known as hydrocortisone). Cortisol synthesis and secretion are under the control of specific hypothalamic and pituitary hormones.7,24 31 Corticotropinreleasing hormone (CRH) from the hypothalamus stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary. ACTH travels in the systemic circulation to reach the adrenal cortex, where it stimulates cortisol synthesis. Cortisol then travels in the bloodstream to various target tissues to exert a number of physiologic effects (see Physiologic Effects of Glucocorticoids, later). 

Enhanced compensatory secretion of adrenocorticotropic hormone (ACTH)... 

Much of this older work must be re-evaluated on the basis of availability of glycogen. A relationship to the adrenal-cortex secretion might be uncovered, but this is a possibility not yet explored. In man, the injection of adrenocorticotropic hormone (ACTH) has been reported not to influence the excretion of (endogenous) glucuronic acid or of hexosamine.176... 

Adrenocorticotropic hormone (Fig. 4) stimulates the cells of the adrenal cortex into the secretion and production of steroid hormones. Conversely, the pituitary secretion of ACTH is inhibited by the adrenal hormones via a feedback mechanism. 

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