Effects of Chaihu Shugan San on behavior and plasma levels of corticotropin releasing hormone and adrenocorticotropic hormone of rats with chronic mild unpredicted stress depression

2009 ◽  
Vol 7 (11) ◽  
pp. 1073-1077 ◽  
Author(s):  
YH Li
Keyword(s):  
Plasma Levels ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Regulation of CRH-induced secretion of ACTH and corticosterone by SOM230 in rats

2005 ◽  
Vol 153 (3) ◽  
pp. R7-R10 ◽  
Author(s):  
A P Silva ◽  
P Schoeffter ◽  
G Weckbecker ◽  
C Bruns ◽  
H A Schmid
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Hormone ◽  
Acth Secretion ◽  
Releasing Hormone ◽  
Corticosterone Secretion ◽  
Corticosterone Release ◽  
Acth Release

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.

Brain oxytocin receptors mediate corticotropin-releasing hormone-induced anorexia

1991 ◽  
Vol 260 (2) ◽  
pp. R448-R452 ◽  
Author(s):  
B. R. Olson ◽  
M. D. Drutarosky ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Food Intake ◽  
Adrenocorticotropic Hormone ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Oxytocin Receptors ◽  
Artificial Cerebrospinal Fluid ◽  
Pituitary Secretion ◽  
Inhibit Food Intake ◽  
Stimulation Of

Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.

Cushingʼs Disease in a Child Caused by a Corticotropin-releasing Hormone-secreting Intrasellar Gangliocytoma Associated with an Adrenocorticotropic Hormone-secreting Pituitary Adenoma

Neurosurgery ◽  
1993 ◽  
Vol 33 (5) ◽  
pp. 920-925 ◽  
Author(s):  
Maximilian J. A. Puchner ◽  
Dieter K. Lüdecke ◽  
José M. Valdueza ◽  
Wolfgang Saeger ◽  
Rolf P. Willig ◽  
...  
Keyword(s):  
Pituitary Adenoma ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Plasma levels of corticotropin-releasing hormone in hypothalamic—pituitary—adrenal disorders and chronic renal failure

1993 ◽  
Vol 128 (6) ◽  
pp. 503-507 ◽  
Author(s):  
Kozo Hashimoto ◽  
Tatsuya Nishioka ◽  
Yukiko Numata ◽  
Takashi Ogasa ◽  
Jingo Kageyama ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Levels ◽  
High Performance ◽  
High Plasma ◽  
Reversed Phase ◽  
Corticotropin Releasing Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
Releasing Hormone ◽  
The Mean

Plasma levels of corticotropin-releasing hormone (CRH) were measured in hypothalamic-pituitary-adrenal disorders and chronic renal failure to investigate the clinical significance of plasma CRH. The mean plasma CRH level in normal subjects (N=26) was 1.64±0.43 pmol/l (normal range 0.77–2.5 pmol/l). Four of six patients with hypothalamic disorders receiving hydrocortisone supplementation had a low plasma CRH level. Two of six patients with Sheehan's syndrome had a low plasma CRH level whereas one patient had a high plasma CRH level. Two patients with Cushing's syndrome had a low plasma CRH level whereas two patients with Cushing's disease had a normal plasma CRH level. Six of 19 patients receiving prednisolone therapy had a low plasma CRH level. The mean plasma CRH level in this group was 0.97±0.34 pmol/l, which is significantly lower than that in the normal group. In this group, significant correlation was seen between plasma CRH and adrenocorticotropin levels. Eleven of 21 patients with chronic renal failure undergoing hemodialysis had a high plasma CRH level. Just after hemodialysis the plasma CRH levels decreased in 15 of 20 patients, while plasma adrenocorticotropin and cortisol levels increased in 13 of 19 patients and in 15 of 20 patients, respectively. Immunoreactive CRH in plasma measured both before and after hemodialysis eluted similarly on reversed-phase high-performance liquid chromatography. These results suggest that the plasma CRH level is at least partially suppressed by a chronically elevated plasma glucocorticoid level and that CRH in plasma is partially removed by hemodialysis.

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