Interactions between CRF, epinephrine, vasopressin and glucocorticoids in the control of acth secretion

Labrie, Fernand; Giguère, Vincent; Proulx, L.; Lefèvre, Gérard

doi:10.1016/0022-4731(84)90202-4

Cited by 48 publications

(21 citation statements)

References 39 publications

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“…Repeated stress affects responsiveness of pituitary corticotropes, an effect depending upon the type of stress and determined by corticotropin-releasing hormone (CRH) and vasopressin (VP) release from the paraventricular nucleus (PVN) in the hypothalamus [6]. CRH is known to regulate pituitary ACTH release [7, 8]and production [9]. VP, a strong osmoregulating hormone mainly synthesized in the magnocellular PVN, was found to be co-localised with CRH in the same vesicles of PVN parvocellular neurons [10]and in the external layer of the median eminence [11].…”

Section: Introductionmentioning

confidence: 99%

Hypothalamo-Pituitary-Adrenal Axis Sensitization after Chronic Salt Loading

Amaya

Tanaka²,

Hayashi³

et al. 2001

Neuroendocrinology

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Hypothalamic parvocellular vasopressin (VP) and corticotropin-releasing hormone (CRH) in the paraventricular nucleus (PVN) are major secretagogues of corticotropin (ACTH), and central plasticity including their alteration is closely related to hypothalamic-pituitary-adrenal (HPA) axis modulation. Chronic hyperosmotic stress caused by 2% salt lodaing has been known to alter VP and CRH expression. We recently reported that rehydration, a recovery stage from salt loading, induced a prolonged increase in parvocellular VP mRNA expression and suggested that rehydration can modulate HPA axis function without obvious external stress. In the present study, we examined hypothalamic VP and CRH mRNA expression and their responsiveness to acute immobilization stress in control, salt-loaded and rehydrated animals, in order to clarify the precise mechanism of HPA axis regulation during rehydration. The results were further compared with plasma corticosterone and ACTH levels. Plasma corticosterone decreased during salt loading, whereas it increased during rehydration at 1 week. Basal ACTH concentration increased in 1-week-rehydrated animals, with enhanced responsiveness to the acute immobilization stress. In the hypothalamic parvocellular PVN, basal CRH mRNA levels also decreased during salt loading and increased during rehydration. Basal VP mRNA was up-regulated during both salt loading and rehydration. VP mRNA responded to additional acute stress during salt loading and rehydration, but CRH mRNA did not. These results indicate that the HPA axis activity of parvocellular neurons is still altered at 1 week of rehydration and that VP plays a dominant role in regulating ACTH release in response to acute stress. This rehydration stage may thus be a good model for analysis of post-stress sensitization of the HPA axis.

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Section: Introductionmentioning

confidence: 99%

Hypothalamo-Pituitary-Adrenal Axis Sensitization after Chronic Salt Loading

Amaya

Tanaka²,

Hayashi³

et al. 2001

Neuroendocrinology

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“…cAMP is increased within the cells and in culture media (Labrie et al, 1984), the CRF effect is duplicated by 8 Br. cAMP and amplified by GTP (Labrie et al, 1984) and phosphodiesterase inhibitors , Vlaskovska et al, 1984 (Eberwine et aL, 1984).…”

Section: Characterization Of 1-41 Crfmentioning

confidence: 99%

“…&horbar;7 contrasts with its action on the pituitary whereby ACTH secretion is stimulated via a! receptors (Labrie et al, 1984) and there is an additive effect on CRF action (Giguere and Labrie, 1983). In turn, CRF stimulates the secretion of both noradrenaline and adrenaline (Brown, Rivier, and Vale, 1984).…”

Section: Characterization Of 1-41 Crfmentioning

confidence: 99%

The physiology of corticotropin-releasing factor (CRF)

Raux-Demay¹,

Girard²

1985

Reprod. Nutr. Dévelop.

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Summary. Corticotropin-releasing Characterization of 1-41 CRFThe purification of ovine CRF ( O CRF) was rapidly followed by the determination of its primary structure and the synthesis of the molecule (Vale et a/., 19811. ).Both extracted and synthetic oCRF's were shown to increase the secretion of ACTH and ¡3-endorphin in vitro in anterior pituitary cell culture and in vivo in rats, and the 10-fold higher activity of the synthetic molecule over natural oCRF has been attributed to the presence of an oxidized methionine residue at C21. oCRF

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“…In vivo studies in rats have suggested that catecholamines secreted from the hypothalamus (3)(4)(5) or peripheral tissues (adrenal medulla and sympathetic nerve endings) may contribute to basal or stress-induced stimulation of ACTH release from the anterior pituitary gland (6)(7)(8). Intravenous administration of low doses of epinephrine stimulates ACTH and corticosterone secretion (7), an effect that was interpreted to be due to direct stimulation of the corticotropic cells in the anterior pituitary gland.…”

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confidence: 99%

Interleukin 1 prevents loss of corticotropic responsiveness to beta-adrenergic stimulation in vitro.

Boyle

Yamamoto

Chen

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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Corticotropin (ACTH) secretion by the anterior pituitary is stimulated by catecholamines in vivo and in vitro. The nature of the response in vivo is controversial but appears to be mediated by .3-adrenergic receptors, whereas the response is dependent on a-adrenergic receptors in cultured anterior pituitary cells. In the present studies, by using a superfusion technique, we demonstrate that catecholamine stimulation of ACTH release from rat anterior pituitaries changes with time from a predominantly P-adrenergicmediated event to a predominantl a-adrenergic-mediated event. From 0 to 2 hr after initiating the superfusion, release of ACTH from anterior pituitary glands is stimulated up to 2.4-fold by the (1wadrenergic agonist l-isoproterenol. However, the ACTH secretory response to the a-adrenergic agonist l-phenylejhrine is -<5% of that to l-isoproterenol during the same time period. Beginning 2 hr after the start of the superfusion, the responsiveness to the fi-adrenergic agonist declines, and the response to the c-adrenergic agonist increases until, 10 hr after removal, >95% of the catecholamineinducible ACTH release is mediated by an a-adrenergic pathway. The addition of interleukin 1 alone to the medium from the beginning of the superfusion does not modify basal ACTH secretion rates and does not affect the acquisition of the response to phenylephrine. However, the presence of interleukin 1 does allow the maintenance of the full ACTH secretory response to isoproterenol. This effect of interleukin 1 is reversed by an interleukin 1 antagonist. These observations suggest an additional way in which immune regulators might interact with the hypothalamic-pituitary-adrenal axis.The secretion of corticotropin (ACTH) by the anterior pituitary gland is regulated by the interaction of several central and peripheral factors including corticotropinreleasing factor (CRF), vasopressin, catecholamines, and glucocorticoids (1, 2). In vivo studies in rats have suggested that catecholamines secreted from the hypothalamus (3-5) or peripheral tissues (adrenal medulla and sympathetic nerve endings) may contribute to basal or stress-induced stimulation of ACTH release from the anterior pituitary gland (6-8). Intravenous administration of low doses of epinephrine stimulates ACTH and corticosterone secretion (7), an effect that was interpreted to be due to direct stimulation of the corticotropic cells in the anterior pituitary gland. This response can be reproduced by the f8-adrenergic agonist 1-isoproterenol and blocked by the p-adrenergic antagonist propranolol (9,10). Administration of high doses of aadrenergic agonists also stimulates ACTH secretion, but this effect may be mediated largely through hypothalamic CRF release (11,12). The effects of a-adrenergic agonists on ACTH (11, 12) or CRF (13) production are reversed by a1-adrenergic antagonists (11-15).In contrast to the situation observed in vivo, in primary cultures of rat anterior pituitary cells, catecholamines alone or in concert with CRF stimulate ACTH release, but...

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Interactions between CRF, epinephrine, vasopressin and glucocorticoids in the control of acth secretion

Cited by 48 publications

References 39 publications

Hypothalamo-Pituitary-Adrenal Axis Sensitization after Chronic Salt Loading

Hypothalamo-Pituitary-Adrenal Axis Sensitization after Chronic Salt Loading

The physiology of corticotropin-releasing factor (CRF)

Interleukin 1 prevents loss of corticotropic responsiveness to beta-adrenergic stimulation in vitro.

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