Adrenocorticotropic Hormone
Adrenocorticotropic hormone (ACTH) is a hormone produced by the pituitary gland that stimulates the adrenal glands to release cortisol and other steroid hormones. It plays a crucial role in the body's response to stress and helps regulate metabolism, immune function, and blood pressure. ACTH levels are controlled by a complex feedback system involving the hypothalamus, pituitary gland, and adrenal glands.
6 Key excerpts on "Adrenocorticotropic Hormone"
eBook - ePubNeurobiology of Depression
Road to Novel Therapeutics
- Joao Quevedo, Andre Ferrer Carvalho, Carlos A. Zarate, Joao Luciano de Quevedo, Andre Ferrer Carvalho, Carlos A. Zarate(Authors)
- 2019(Publication Date)
- Academic Press(Publisher)
...This triggers the subsequent release of Adrenocorticotropic Hormone (ACTH) from the anterior pituitary gland, leading to the production and secretion of glucocorticoids (cortisol and corticosterone) by the adrenal cortex. In addition, the adrenal medulla releases catecholamines (adrenalin and noradrenalin) (not shown). The responsiveness of the HPA axis to stressors is in part determined by the ability of glucocorticoids to regulate ACTH- and CRH-release by binding to two corticosteroid receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). Following activation of the system, and once the perceived stressor has subsided, feedback loops are triggered at various levels of the system (adrenal gland, pituitary, hypothalamus, and other brain regions such as the hippocampus and the frontal cortex) in order to shut down the HPA axis and return to a set homeostatic point. In contrast, the amygdala activates the HPA axis to set in motion the stress response that is necessary to deal with the challenge (not shown). (Figure designed by Dorothea Ziemens.) The HPA axis can be dissected into the central (neuropeptide) components and the related peripheral (endocrine) organs [1, 2, 8]. Corticotropin-releasing hormone (CRH) regulates both the basal and the stress-induced release of Adrenocorticotropic Hormone (ACTH) from the anterior lobe of the pituitary. CRH is also implicated in other stress response components, such as arousal and autonomic activity [2, 9, 10]. Therefore, the CRH-producing parvocellular neurons of the paraventricular nucleus (PVN) of the hypothalamus can be regarded as focal point for modulating HPA axis activity. Furthermore, the PVN's central role in integrating information relevant for eliciting the stress response is also evidenced by its multiple connections to other brain structures implicated in emotion and cognition...
eBook - ePubHormone/Behavior Relations of Clinical Importance
Endocrine Systems Interacting with Brain and Behavior
- Robert H. Rubin, Donald W. Pfaff, Robert H. Rubin, Donald W. Pfaff(Authors)
- 2010(Publication Date)
- Academic Press(Publisher)
...As part of the HPA axis, ACTH is considered as one of the major stress hormones. It is now apparent that AVP and CRH cooperate as the major factors involved in the control of ACTH release. 2.1.6 Glucocorticoids The zona fasciculata cells of the adrenal cortex synthesize and secrete glucocorticoids in response to ACTH secreted by the anterior pituitary (Jacobson, 2005). Glucocorticoids, cortisol in humans and corticosterone in rodents, are the final effectors of the HPA axis. Stimulation of the HPA axis causes secretion of glucocorticoid hormones which act in the brain and periphery to promote adaptation to allostasis (Herman and Seroogy, 2006). These hormones exert a multitude of functions that affect virtually every cell in the body and exert their effects through their ubiquitously distributed intracellular receptors. Glucocorticoids function primarily to redistribute energy resources and are intimately involved in restoration or defense of homeostasis after challenge (Herman and Seroogy, 2006 ; Jacobson, 2005). Glucocorticoids play an important role in energy mobilization because they stimulate gluconeogenesis, which promotes lipolysis and an increase in protein catabolism (Mastorakos et al., 2005). Glucocorticoids also act within the brain to increase appetite as well as locomotor and food-seeking activities, which are important behaviors influencing energy expenditure (McEwen, 2000). In addition, these hormones play a key regulatory role in the regulation of HPA-axis activity and in the termination of the stress response by acting, via negative-feedback loops, on the hypothalamus as well as extrahypothalamic regulatory centers, such as the hippocampus, frontal complex, and pituitary gland (Chrousos, 2000a ; Gabry et al., 2002). Circulation of glucocorticoids occurs by low-affinity binding to albumin and by high-affinity binding to corticosteroid-binding globulin...
eBook - ePub- Steven L. Stockham, Michael A. Scott(Authors)
- 2013(Publication Date)
- Wiley-Blackwell(Publisher)
...Regulation of cortisol and aldosterone secretion (Fig. 18.1) A. CRH from the hypothalamus stimulates the production and release of pituitary ACTH and other hormones. Low [cortisol] promotes secretion of CRH and ACTH. High [cortisol] inhibits secretion of CRH and ACTH. B. ACTH stimulates the production and release of cortisol, aldosterone, and other steroid compounds from the adrenal glands. The adrenal gland cortices produce most circulating cortisol. C. Aldosterone secretion is also stimulated by angiotensin II, hyperkalemia, and hyponatremia but is inhibited by atrial natriuretic peptide. The secreted aldosterone stimulates the renal retention of Na + and Cl − and excretion of K + and H +. D. Peak secretion of cortisol occurs in the morning in dogs and horses but in the evening in cats. The degree of daily variation is minimal in domestic mammals 1 but may need to be considered when interpreting diagnostic tests in horses (average about 3.0 μg/dL at midnight; averages 4.5–5.0 μg/dL from 8 a.m. to 4 p.m.). 2 E. Nearly all cortisol released from the adrenal glands becomes bound to plasma proteins. 1 In dogs, about 40 % of cortisol is bound to transcortin, 50 % to albumin, and the remainder (5–10 %) is free. The half-life of cortisol is about 1.5 h in dogs and less in cats. F. Cortisol binds to receptor proteins in cells. The cortisol-receptor complex initiates synthesis of hormone and cytokine receptors and other proteins involved in gluconeogenesis, protein catabolism, lipolysis, immune responses, and H 2 O balance. G. Most cortisol is removed from plasma by hepatocytes, but there is also urinary excretion of cortisol and cortisol metabolites. Fig. 18.1. Regulation of cortisol and aldosterone secretion. CRH released from the hypothalamus stimulates the production and release of ACTH from the pituitary gland. ACTH stimulates the production and release of cortisol and aldosterone from the adrenal gland cortices...
eBook - ePub- François-René Bertin, Natalie S Fraser(Authors)
- 2020(Publication Date)
- CAB International(Publisher)
...Many types of cell express glucocorticoid receptors and cortisol plays a paramount role in the response to stress, increasing blood pressure, improving tissue perfusion and regulating inflammation (Hurcombe et al., 2008; Hoffman et al., 2015; Stewart et al., 2019b). Another key role of cortisol is the regulation of the hypothalamo–pituitary–adrenocortical axis itself as cortisol is a potent down regulator of CRH secretion by the hypothalamus, of ACTH secretion by the pituitary gland and of mineralocorticoids, glucocorticoids and androgens secretion by the adrenal cortex. Androgens are mainly secreted by testicles in males but in females they are predominantly secreted by the zona reticularis of the adrenal gland under ACTH stimulation. Androstenedione is metabolized into oestrogen and testosterone, which play a role in sexual development during puberty (Hart and Barton, 2011). Dopamine, a peptide hormone of the catecholamine family, is the main melanotrope regulator. Released by hypothalamic nerves, dopamine interacts with dopamine D2 receptors on melanotropes located in the pars intermedia of the pituitary gland, to limit their proliferation and the synthesis and secretion of POMC (Saiardi and Borrelli, 1998). Another regulator of POMC secretion by melanotropes of clinical interest is the thyrotropin-releasing hormone (TRH) (McFarlane et al., 2006). Although both corticotropes and melanotropes secrete POMC, post-translational processing of the peptide differs. While corticotropes mainly express prohormone convertase 1 leading to the secretion of a large amount of ACTH, melanotropes express prohormone convertase 1 and prohormone convertase 2 leading to the secretion of smaller amounts of ACTH and a larger amount of α-MSH and CLIP (Fig. 4.1(B)) (McFarlane, 2011). The physiological role of α-MSH and CLIP is unclear...
- Linas A Bieliauskas(Author)
- 2019(Publication Date)
- Routledge(Publisher)
...2 Hormonal Responses to Stress The Complexity of Hormonal Stress Responses Selye (1952) initially described the biological stress response as follows: The presence of a stressor (through imperfectly understood mechanisms) acts upon the anterior pituitary and stimulates the secretion of somatotropic (STH) and adrenocorticotropic (ACTH) hormones. Although STH acts to stimulate the growth of the body in general, and the growth of thymicolymphatic tissue in particular, it also stimulates the growth of connective tissue to repair physical damage and raises the inflammation potential of the organism to help prevent infiltration by a foreign pathogen. The action of STH can be classified as primarily prophlogistic, that is, it augments inflammation and combats the pathogen. ACTH, on the other hand, stimulates the adrenal cortex to produce two classes of hormones, the mineralocorticoids and the glucocorticoids (Selye, 1952). The mineralocorticoids are classified as prophlogistic corticoids (PC) because they mimic the effect of STH in response to a stressor: they increase inflammation and promote connective tissue proliferation. However, as we noted in Chapter 1, extended prophlogistic reaction -such as a high fever (inflammation reaction)-may threaten the life of the organism. Therefore, if PC action cannot ade quately control a stressor, that action must be terminated lest serious consequences result. According to Selye (1956), overextended prophlogistic activity may cause nephrosclerosis, hypertension, and allergic reactions. The glucocorticoids are classified as antiphlogistic corticoids (AC) in that they are anti-inflammatory and thus inhibit PC aggrandizement. AC action is initiated as PC-affected tissue becomes increasingly sensitive to the ACs. Selye (1950) called this antiphlogistic response "adaptation." Because ACTH secretion is necessary for AC production, ACTH is generally classified as antiphlogistic...
eBook - ePubAdrenal Cortex
Butterworths International Medical Reviews: Clinical Endocrinology
- David C. Anderson, Jeremy S. D. Winter, David C. Anderson, Jeremy S. D. Winter(Authors)
- 2013(Publication Date)
- Butterworth-Heinemann(Publisher)
...This implies that corticotrophs have a functional defect or that excessive ACTH secretion can occur without morphological evidence of hyperplasia as a result of hypothalamic stimulation. (3) Hyperplasia of corticotrophs with or without a tumour in either the anterior pituitary or the zone between the anterior and posterior pituitary (intermediate lobe-like cells). Anterior lobe hyperplasia implies stimulation by hypothalamic releasing factors, while hyperplasia and/or nodules in the intermediate zone may imply a different pathogenesis since these cells may be controlled by neural factors and show relative resistance to classical corticosteroid negative feedback. Indeed, in some cases argyrophil nerve fibres have been demonstrated to course freely through adenoma tissue and end apparently around individual adenoma cells (Lamberts, de Lange and Stefanko, 1982). Several potential neurotransmitters may be involved – catecholamines (noradrenaline and dopamine), serotonin, acetylcholine, γ-aminobutyric acid (GABA), vasopressin and opioid and other peptides. Their role in controlling ACTH secretion of either anterior or intermediate lobe corticotrophs is uncertain although there is evidence that bromocriptine (a dopamine agonist) and cyproheptadine (a serotonin antagonist) can inhibit ACTH secretion, at least in the short term in some cases of Cushing’s disease (Lamberts et al, 1977 ; Krieger, Amorosa and Linick, 1975) and that valproate (a GABA agonist) can reduce ACTH levels in some cases of Nelson’s syndrome (Dornhurst et al., 1983). It has also been reported that thyrotropin-releasing factor (TRF) and/or luteinizing hormone releasing factor (LH-RF) stimulate ACTH and cortisol responses acutely in a variable proportion of patients with Cushing’s disease (Pieters et al., 1982b). In this context, TRF can stimulate ACTH and cortisol release in pregnant women, suggesting that functioning intermediate lobe tissue is required for the effect...
