The role of hypothalamic catecholamines in the regulation of ACTH secretion in the rat

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S129
Author(s):  
H. LEHNERT ◽  
J. BEYER ◽  
U. KRAUSE ◽  
D.K. REINSTEIN ◽  
R.J. WURTMAN
Keyword(s):  
Acth Secretion

The Role of Pineal Principles in the Control of ACTH Secretion

1973 ◽  
pp. 231-236 ◽  
Author(s):  
F. Piva ◽  
O. Schiaffini ◽  
M. Motta ◽  
L. Martini
Keyword(s):  
Acth Secretion

scholarly journals Ubiquitin-Specific Protease 8 Mutant Corticotrope Adenomas Present Unique Secretory and Molecular Features and Shed Light on the Role of Ubiquitylation on ACTH Processing

2019 ◽  
Vol 110 (1-2) ◽  
pp. 119-129 ◽  
Author(s):  
Antonella Sesta ◽  
Maria Francesca Cassarino ◽  
Mariarosa Terreni ◽  
Alberto G. Ambrogio ◽  
Laura Libera ◽  
...  
Keyword(s):  
Protein Degradation ◽  
Pituitary Adenomas ◽  
Expression Profiles ◽  
Primary Cultures ◽  
Acth Secretion ◽  
Specific Protease ◽  
Ubiquitin Proteasome ◽  
Ubiquitin Specific Protease ◽  
Acth Secreting

Background: Somatic mutations in the ubiquitin-specific protease 8 (USP8) gene have recently been shown to occur in ACTH-secreting pituitary adenomas, thus calling attention to the ubiquitin system in corticotrope adenomas. Objectives: Assess the consequences of USP8 mutations and establish the role of ubiquitin on ACTH turnover in human ACTH-secreting pituitary adenomas. Methods: USP8 mutation status was established in 126 ACTH-secreting adenomas. Differences in ACTH secretion and POMC expression from adenoma primary cultures and in microarray gene expression profiles from archival specimens were sought according to USP8 sequence. Ubiquitin/ACTH coimmunoprecipitation and incubation with MG132, a proteasome inhibitor, were performed in order to establish whether ubiquitin plays a role in POMC/ACTH degradation in corticotrope adenomas. Results: USP8 mutations were identified in 29 adenomas (23%). Adenomas presenting USP8 mutations secreted greater amounts of ACTH and expressed POMC at higher levels compared to USP wild-type specimens. USP8 mutant adenomas were also more sensitive to modulation by CRH and dexamethasone in vitro. At microarray analysis, genes associated with endosomal protein degradation and membrane components were downregulated in USP8 mutant adenomas as were AVPR1B, IL11RA, and PITX2. Inhibition of the ubiquitin-proteasome pathway increased ACTH secretion and POMC itself proved a target of ubiquitylation, independently of USP8 sequence status. Conclusions: Our study has shown that USP8 mutant ACTH-secreting adenomas present a more “typical” corticotrope phenotype and reduced expression of several genes associated with protein degradation. Further, ubiquitylation is directly involved in intracellular ACTH turnover, suggesting that the ubiquitin-proteasome system may represent a target for treatment of human ACTH-secreting adenomas.

Neuroendocrine and cardiovascular effects of serotonin: selective role of brain angiotensin on vasopressin

1996 ◽  
Vol 270 (3) ◽  
pp. E513-E521 ◽  
Author(s):  
J. A. Saydoff ◽  
P. A. Rittenhouse ◽  
M. Carnes ◽  
J. Armstrong ◽  
L. D. Van De Kar ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Cardiovascular Effects ◽  
Intraventricular Injection ◽  
Intracerebroventricular Injection ◽  
Ang Ii ◽  
Acth Secretion ◽  
At1 Antagonist ◽  
Neuroendocrine Activation ◽  
Ly 53857

Central serotonin (5-HT) and angiotensin (ANG II) stimulate arginine vasopressin (AVP), oxytocin (OT), and adrenocorticotropin (ACTH) secretion and increase blood pressure. Studies were conducted in conscious rats to determine whether neuroendocrine activation by 5-HT requires a brain angiotensinergic intermediate pathway. In the first study, ANG II formation was inhibited by the angiotensin-converting enzyme inhibitor enalapril before injection of the 5-HT releaser/uptake inhibitor d-fenfluramine. Fenfluramine (2 mg/kg ip) stimulated AVP, OT, corticosterone, and prolactin (PRL) secretion (P<0.01). Enalapril (60 mg/l in drinking water for 4 days and 10 mg/kg ip 2 h before the rats were killed) inhibited only the AVP response (P<0.01) to d-fenfluramine. In the second study, the effect of intracerebroventricular injection of the 5-HT2A/2C antagonist LY-53857 (10 microgram), or the ANG II AT1 antagonist DuP-753 (10 microgram), on intracerebroventricular 5-HT (10 microgram)-stimulated AVP, OT, ACTH, PRL, renin secretion, mean arterial pressure (MAP) and heart rate (HR) was tested. LY-53857 inhibited the AVP, OT, and ACTH responses to 5-HT (P<0.01), whereas DuP-753 inhibited only the AVP response (P<0.01). Intraventricular injection of 5-HT increased MAP and decreased HR. The MAP response was not affected by LY-53857 or DuP-753, and at no time did MAP decline below starting levels. The decreased HR was inhibited by LY-53857 but not by DuP-753. These results demonstrate that 5-HT-induced AVP secretion is mediated selectively via brain angiotensinergic mechanisms by way of the AT1 receptor.

The role of integrated 18F-FDG PET/CT in identification of ectopic ACTH secretion tumors

Endocrine ◽  
2009 ◽  
Vol 36 (3) ◽  
pp. 385-391 ◽  
Author(s):  
Haoping Xu ◽  
Min Zhang ◽  
Ge Zhai ◽  
Miao Zhang ◽  
Guang Ning ◽  
...  
Keyword(s):  
Fdg Pet ◽  
Acth Secretion ◽  
Ectopic Acth ◽  
Ectopic Acth Secretion ◽  
Pet Ct ◽  
18F Fdg ◽  
Fdg Pet Ct

Effect of brain monoamines on the secretion of adrenocorticotrophic hormone

1982 ◽  
Vol 101 (2) ◽  
pp. 180-186 ◽  
Author(s):  
Alka Amar ◽  
S. Mandal ◽  
A. K. Sanyal
Keyword(s):  
Dopaminergic Neurons ◽  
Adrenal Glands ◽  
Plasma Corticosterone ◽  
Albino Rats ◽  
Adrenocorticotrophic Hormone ◽  
Brain Monoamines ◽  
Acth Secretion ◽  
Acute Increase

Abstract. The role of brain monoamines (5-HT, NA and DA) in the secretion of adrenocorticotrophic hormone (ACTH) was studied in view of contradictory reports. Plasma corticosterone levels and the rate of synthesis of corticosterone in vitro by the adrenal gland were estimated in albino rats and have been taken as the index of ACTH activity. These estimations were done in unstressed and stressed, and in untreated and treated rats. Drugs were administered intracerebroventricularly to the rats to cause selective degeneration of tryptaminergic, noradrenergic or dopaminergic neurons. The results show that plasma corticosterone levels and the rate of synthesis of corticosterone were significantly decreased after selective degeneration of tryptaminergic neurons in unstressed rats. After selective degeneration of either tryptaminergic or noradrenergic neurons, the acute increase in the plasma corticosterone levels and rate of synthesis of corticosterone in vitro by adrenal glands in stressed rats were significantly inhibited. These results have been interpreted to suggest that the central tonic control on adrenal glands may be 5-HT mediated and that during stress ACTH secretion may be both 5-HT and NA mediated. DA does not seem to have significant role in the regulation of ACTH secretion.

Vasopressin: a regulator of adrenal glucocorticoid production?

1989 ◽  
Vol 256 (4) ◽  
pp. E566-E572
Author(s):  
V. L. Brooks ◽  
L. J. Blakemore
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Acth Secretion ◽  
Vasopressin Infusion ◽  
Plasma Cortisol Concentration ◽  
Glucocorticoid Response ◽  
Acth Concentration ◽  
Glucocorticoid Production ◽  
Adrenal Glucocorticoid ◽  
Sustained Increase

Vasopressin infusion has been shown to decrease plasma adrenocorticotropic hormone (ACTH) concentration and transiently increase plasma cortisol concentration in conscious dogs. In the present study, one experiment tested the hypothesis that vasopressin infusion decreases ACTH by activation of a V1 receptor mechanism, e.g., by increasing atrial pressures and stimulating the low-pressure baroreceptor reflex. Administration of a vasopressin V1 antagonist eliminated the increases in atrial pressure and decreases in heart rate with vasopressin infusion (1 ng.kg-1.min-1), as it eliminated the decrease in ACTH, which is consistent with baroreflex-mediated inhibition of ACTH by vasopressin. A second experiment evaluated the role of ACTH in the increase in glucocorticoids. Dexamethasone pretreatment, which inhibits ACTH secretion, abolished the increase in glucocorticoid concentration with vasopressin infusion, indicating that ACTH is necessary for the glucocorticoid response. A third experiment was performed to determine whether the glucocorticoid response could be restored in dexamethasone-treated dogs, when ACTH concentration was maintained near control levels by intravenous infusion of synthetic alpha-ACTH-(1-24) (0.3 ng.kg-1.min-1). In these dogs, vasopressin infusion produced a sustained increase in plasma glucocorticoid concentration from 22 +/- 3 to 49 +/- 8 ng/ml (P less than 0.001). Infusing higher levels of ACTH (0.5 ng.kg-1.min-1) enhanced basal glucocorticoid levels but did not enhance the response to vasopressin. Vasopressin infusion did not alter clearance of glucocorticoids. Collectively, these results suggest that vasopressin directly stimulates adrenal glucocorticoid production, provided that background levels of ACTH are present.

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