CORTICOTROPIN-RELEASING HORMONE (CRH) DIRECTLY STIMULATES CORTICOSTERONE SECRETION BY THE RAT ADRENAL GLAND

Endocrinology ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 1198-1200 ◽  
Author(s):  
Paola G. Andreis ◽  
Giuliano Neri ◽  
Gastone G. Nussdorfer
2005 ◽  
Vol 153 (3) ◽  
pp. R7-R10 ◽  
Author(s):  
A P Silva ◽  
P Schoeffter ◽  
G Weckbecker ◽  
C Bruns ◽  
H A Schmid

Objective: Adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome is biochemically characterized by increased plasma concentrations of ACTH inducing hypersecretion of cortisol. Somatostatin is known to inhibit ACTH secretion, and in vitro data have shown the inhibition of ACTH secretion by agonists activating sst2 and sst5 receptors. The present study aimed to determine the inhibitory effect of the multireceptor ligand SOM230, compared with the sst2-preferring agonist octreotide, on corticotropin-releasing hormone (CRH)-stimulated secretion of ACTH and corticosterone in rats. Methods: Secretion of ACTH and corticosterone was induced by i.v. application of CRH (0.5 μg/kg) in rats pretreated 1 h before by i.v. application of SOM230 (1, 3, or 10 μg/kg), octreotide (10 μg/kg) or NaCl 0.9%. Results: SOM230 (3 and 10 μg/kg) inhibited CRH-induced ACTH release by 45±3% and 51±2%, respectively, and corticosterone release by 43±5% and 27±16%, respectively. 10 μg/kg of octreotide tended to be less potent at inhibiting ACTH release (34±6% inhibition) and did not alter the secretion of corticosterone. Conclusion: SOM230 has a stronger inhibitory effect on ACTH and corticosterone secretion than octreotide in rats. This difference can be explained by its higher affinity to sst1, sst3 and especially sst5 receptors compared with octreotide.


2001 ◽  
pp. 131-141
Author(s):  
Andrew N. Margioris ◽  
Erene Dermitzaki ◽  
Maria Venihaki ◽  
Achille Gravanis

2011 ◽  
Vol 172 (3) ◽  
pp. 416-422 ◽  
Author(s):  
Caterina Squillacioti ◽  
Adriana De Luca ◽  
Giovanna Liguori ◽  
Salvatore Paino ◽  
Nicola Mirabella

2003 ◽  
Vol 61 (3) ◽  
pp. 308-314 ◽  
Author(s):  
Ilias Vrezas ◽  
Holger S. Willenberg ◽  
Georg Mansmann ◽  
Naoki Hiroi ◽  
Reimar Fritzen ◽  
...  

1993 ◽  
Vol 4 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Francesco G. Musajo ◽  
Ludwik K. Malendowicz ◽  
Paola G. Andreis ◽  
Gastone G. Nussdorfer

1994 ◽  
Vol 5 (4) ◽  
pp. 345-349 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Ludwick K. Malendowicz ◽  
Anna Markowska ◽  
Gastone G. Nussdorfer

2021 ◽  
Vol 22 (18) ◽  
pp. 9908
Author(s):  
Willian O. dos Santos ◽  
Daniela O. Gusmao ◽  
Frederick Wasinski ◽  
Edward O. List ◽  
John J. Kopchick ◽  
...  

Corticotropin-releasing hormone (CRH) cells are the dominant neuronal population responsive to the growth hormone (GH) in the paraventricular nucleus of the hypothalamus (PVH). However, the physiological importance of GH receptor (GHR) signaling in CRH neurons is currently unknown. Thus, the main objective of the present study was to investigate the consequences of GHR ablation in CRH-expressing cells of male and female mice. GHR ablation in CRH cells did not cause significant changes in body weight, body composition, food intake, substrate oxidation, locomotor activity, glucose tolerance, insulin sensitivity, counterregulatory response to 2-deoxy-D-glucose and ghrelin-induced food intake. However, reduced energy expenditure was observed in female mice carrying GHR ablation in CRH cells. The absence of GHR in CRH cells did not affect anxiety, circadian glucocorticoid levels or restraint-stress-induced corticosterone secretion and activation of PVH neurons in both male and female mice. In summary, GHR ablation, specifically in CRH-expressing neurons, does not lead to major alterations in metabolism, hypothalamic–pituitary–adrenal axis, acute stress response or anxiety in mice. Considering the previous studies showing that central GHR signaling regulates homeostasis in situations of metabolic stress, future studies are still necessary to identify the potential physiological importance of GH action on CRH neurons.


1998 ◽  
Vol 68 (2) ◽  
pp. 116-122 ◽  
Author(s):  
Margarita M. Garrido ◽  
Sonsoles Martin ◽  
Emilio Ambrosio ◽  
José A. Fuentes ◽  
Jorge Manzanares

Sign in / Sign up

Export Citation Format

Share Document