Role of the Hypothalamus in the Regulation of ACTH Release

2015 ◽  
pp. 177-195 ◽  
Author(s):  
A. Brodish
Keyword(s):  
Acth Release

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

2007 ◽  
Vol 292 (1) ◽  
pp. R497-R504 ◽  
Author(s):  
Nao Ohiwa ◽  
Hyukki Chang ◽  
Tsuyoshi Saito ◽  
Tatsushi Onaka ◽  
Takahiko Fujikawa ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Metabolic Response ◽  
Ventrolateral Medulla ◽  
Hypothalamic Nucleus ◽  
Dependent Manner ◽  
Lactate Accumulation ◽  
Blood Lactate Accumulation ◽  
Prolactin Releasing Peptide ◽  
Acth Release

Exercise around the lactate threshold induces a stress response, defined as “running stress.” We have previously demonstrated that running stress is associated with activation of certain regions of the brain, e.g., the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus, that are hypothesized to play an integral role in regulating stress-related responses, including ACTH release during running. Thus we investigated the role of prolactin-releasing peptide (PrRP), found in the ventrolateral medulla and the nucleus of the solitary tract, which is known to project to the PVN during running-induced ACTH release. Accumulation of c-Fos in PrRP neurons correlated with running speeds, reaching maximal levels under running stress. Intracerebroventricular injection of neutralizing anti-PrRP antibodies led to increased plasma ACTH level and blood lactate accumulation during running stress, but not during restraint stress. Exogenous intracerebroventricular administration of low doses of PrRP had the opposite effects. Therefore, our results suggest that, during running stress, PrRP-containing neurons are activated in an exercise intensity-dependent manner, and likewise the produced endogenous PrRP attenuates ACTH release and blood lactate accumulation during running stress. Here we provide a novel perspective on understanding of PrRP in the endocrine-metabolic response associated with running stress.

The role of vasotocin and of CRF in ACTH release in the chicken

1970 ◽  
Vol 14 (2) ◽  
pp. 281-289 ◽  
Author(s):  
M.H.M. Salem ◽  
H.W. Norton ◽  
A.V. Nalbandov
Keyword(s):  
Acth Release

Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

2007 ◽  
Vol 292 (1) ◽  
pp. E7-E15 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Rodrigo Alvear-Perez ◽  
Philippe Zizzari ◽  
Jacques Epelbaum ◽  
Marie-Thérèse Bluet-Pajot ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Cellular Localization ◽  
Physiological Role ◽  
Nerve Fibers ◽  
Male Rat ◽  
Stimulatory Action ◽  
Receptor Mrna ◽  
Apelin Receptor ◽  
Acth Release

Apelin is a bioactive peptide recently identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ. The presence of apelin-immunoreactive nerve fibers, together with the detection of apelin receptor mRNA in the parvocellular part of the paraventricular nucleus and the stimulatory action of apelin on corticotropin-releasing hormone release, indicate that apelin modulates adrenocorticotropin (ACTH) release via an indirect action on the hypothalamus. However, a direct action of apelin in the anterior pituitary cannot be excluded. Here, we provided evidence for the existence of an apelinergic system within the adult male rat pituitary gland. Double immunofluorescence staining indicated that apelin is highly coexpressed in the anterior pituitary, mainly in corticotrophs (96.5 ± 0.3%) and to a much lower extent in somatotropes (3.2 ± 0.2%). Using in situ hybridization combined with immunohistochemistry, a high expression of apelin receptor mRNA was also found in corticotrophs, suggesting a local interaction between apelin and ACTH. In an ex vivo perifusion system of anterior pituitaries, apelin 17 (K17F, 10−6 M) significantly increased basal ACTH release by 41%, whereas apelin 10 (R10F, 10−6 M), an inactive apelin fragment, was ineffective. In addition, K17F but not R10F induced a dose-dependent increase in K+-evoked ACTH release, with maximal increase being observed for a 10−6 M concentration. Taken together, these data outline the potential role of apelin as an autocrine/paracrine-acting peptide on ACTH release and provide morphological and neuroendocrine basis for further studies that explore the physiological role of apelin in the regulation of anterior pituitary functions.

Role of Oxytocin in the Modulation of ACTH Release in Women

1986 ◽  
Vol 44 (3) ◽  
pp. 309-313 ◽  
Author(s):  
Bo Y. Suh ◽  
James H. Liu ◽  
Dennis D. Rasmussen ◽  
Daniel M. Gibbs ◽  
Jeff Steinberg ◽  
...  
Keyword(s):  
Acth Release

Defective interleukin-1-induced ACTH release in cholestatic rats: impaired hypothalamic PGE2 release

1995 ◽  
Vol 268 (3) ◽  
pp. G404-G409 ◽  
Author(s):  
M. G. Swain ◽  
M. Maric ◽  
L. Carter
Keyword(s):  
Bile Duct ◽  
Hpa Axis ◽  
Interleukin 1 ◽  
Proinflammatory Mediators ◽  
Significant Attenuation ◽  
Regulatory Loop ◽  
Hypothalamic Level ◽  
Acth Release

A complete regulatory loop exists between the immune and neuroendocrine systems. Proinflammatory mediators such as endotoxin (lipopolysaccharide) and interleukin-1 (IL-1) are capable of activating the hypothalamic-pituitary-adrenal (HPA) axis at the hypothalamic level, presumably by inducing the synthesis of prostaglandins. We have recently identified abnormalities in the stress-induced activation of the HPA axis in cholestatic rats. Therefore, in rats with cholestasis due to bile duct resection and sham-resected controls, we studied alterations in proinflammatory mediator-induced activation of the HPA axis and documented the role of alterations in hypothalamic prostaglandin synthesis in these abnormalities. Systemic administration of endotoxin and IL-1 resulted in a significant attenuation of adrenocorticotropic hormone (ACTH) release into plasma in bile duct-resected compared with sham-resected animals. This suppression of endotoxin- or IL-1-induced ACTH release in bile duct-resected rats was associated with a complete absence of IL-1-induced hypothalamic release of prostaglandin E2 (PGE2) in vitro in these animals. In contrast, sham-resected rats exhibited a 70% increase in hypothalamic PGE2 secretion in vitro in response to IL-1. However, bile duct-resected rats exhibited HPA axis activation similar to that of sham-resected animals in response to intracerebroventricularly infused PGE2. Therefore, cholestasis in the rat is associated with an attenuation of central activation of the HPA axis by proinflammatory mediators that appears to be mediated, at least in part, by defective IL-1-induced hypothalamic prostaglandin production.

Role of vasopressin in stimulation of ACTH secretion by angiotensin II in conscious dogs

1986 ◽  
Vol 251 (1) ◽  
pp. E52-E57
Author(s):  
C. K. Klingbeil ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Conscious Dogs ◽  
Ang Ii ◽  
Acth Secretion ◽  
Series Of Experiments ◽  
Stimulation Of ◽  
Acth Release

Three series of experiments were performed in conscious dogs to test the possibility that the stimulation of adrenocorticotropin (ACTH) release by angiotensin II (ANG II) is mediated by arginine vasopressin (AVP). In the first protocol, the effect of ANG II on ACTH release was studied in dogs in which endogenous AVP levels had been increased by water deprivation. Water deprivation for 24 h increased plasma AVP concentration from 3.0 +/- 0.5 to 7.7 +/- 0.5 pg/ml (P less than 0.01) and increased the AVP response to the highest dose of ANG II (20 ng X kg-1 X min-1). Despite these changes, water deprivation failed to increase the ACTH response to ANG II. Next, the contribution of endogenous AVP to the stimulation of ACTH release by ANG II was examined using the V1-receptor antagonist, d(CH2)5Tyr[Met]-AVP (10 micrograms/kg iv). The ACTH response to ANG II in the presence of the AVP antagonist (66.4 +/- 3.1 to 100.1 +/- 15.9 pg/ml) was not significantly less than that in its absence (53.0 +/- 4.8 to 72.2 +/- 11.1 pg/ml). Finally, ANG II and AVP were infused in combination to determine whether there is a synergism between these two peptides in the release of ACTH. In one protocol, AVP and ANG II were infused separately and in combination. The ACTH response to ANG II and AVP in combination (48.7 +/- 6.5 to 61.5 +/- 8.5 pg/ml) was not enhanced compared with the responses to ANG II (59.8 +/- 7.3 to 71.0 +/- 10.1 pg/ml) or AVP (48.8 +/- 5.7 to 55.6 +/- 6.5 pg/ml) alone.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells

2005 ◽  
Vol 289 (2) ◽  
pp. E278-E287 ◽  
Author(s):  
Joost van der Hoek ◽  
Marlijn Waaijers ◽  
Peter M. van Koetsveld ◽  
Diana Sprij-Mooij ◽  
Richard A. Feelders ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Binding Affinity ◽  
Binding Capacity ◽  
Somatostatin Receptor ◽  
Inhibitory Effect ◽  
Pcr Analysis ◽  
Receptor Subtype ◽  
Mrna Levels ◽  
Acth Release

In a series of human corticotroph adenomas, we recently found predominant mRNA expression of somatostatin (SS) receptor subtype 5 (sst5). After 72 h, the multiligand SS analog SOM230, which has a very high sst5 binding affinity, but not Octreotide (OCT), significantly inhibited basal ACTH release. To further explore the role of sst5 in the regulation of ACTH release, we conducted additional studies with mouse AtT-20 cells. SOM230 showed a 7-fold higher ligand binding affinity and a 19-fold higher potency in stimulating guanosine 5′- O-(3-thiotriphosphate) binding in AtT-20 cell membranes compared with OCT. SOM230 potently suppressed CRH-induced ACTH release, which was not affected by 48-h dexamethasone (DEX) pretreatment. However, DEX attenuated the inhibitory effects of OCT on ACTH release, whereas it increased the inhibitory potency of BIM-23268, an sst5-specific analog, on ACTH release. Quantitative PCR analysis showed that DEX lowered sst2A+2B mRNA expression significantly after 24 and 48 h, whereas sst5 mRNA levels were not significantly affected by DEX treatment. Moreover, Scatchard analyses showed that DEX suppressed maximum binding capacity (Bmax) by 72% when 125I-Tyr3-labeled OCT was used as radioligand, whereas Bmax declined only by 17% when AtT-20 cells were treated with [125I-Tyr11]SS-14. These data suggest that the sst5 protein, compared with sst2, is more resistant to glucocorticoids. Finally, after SS analog preincubation, compared with OCT both SOM230 and BIM-23268 showed a significantly higher inhibitory effect on CRH-induced ACTH release. In conclusion, our data support the concept that the sst5 receptor might be a target for new therapeutic agents to treat Cushing’s disease.

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