Dual Control of ACTH Secretion by Hypothalamic and Placental Corticotropin-Releasing Factor (CRF) in Late Pregnancy

1989 ◽  
pp. 303-307
Author(s):  
B. Allolio ◽  
H. M. Schulte ◽  
J. Hoffmann ◽  
M. Kusche ◽  
W. Winkelmann ◽  
...  
Keyword(s):  
Late Pregnancy ◽  
Corticotropin Releasing Factor ◽  
Dual Control ◽  
Acth Secretion

Regulation of bioactive and immunoreactive ACTH secretion by CRF and AVP in sheep fetuses

1995 ◽  
Vol 269 (6) ◽  
pp. E1076-E1082 ◽  
Author(s):  
T. J. Zehnder ◽  
N. K. Valego ◽  
J. Schwartz ◽  
A. White ◽  
J. C. Rose
Keyword(s):  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Factor ◽  
Acth Secretion ◽  
Fetal Sheep

The purpose of this study was to determine the effects of corticotropin-releasing factor (CRF) or arginine vasopressin (AVP) on the secretion of bioactive adrenocorticotropic hormone (bACTH) and immunoreactive ACTH (iACTH), the latter being measured by radioimmunoassay and separate two-site immunoradiometric assays for ACTH-(1-39) and ACTH precursors. Experiments were performed on chronically catheterized fetal sheep at 0.70 (n = 9) and 0.90 (n = 8) gestation. Each fetus received a 15-min infusion of CRF, AVP, or saline on 3 consecutive days. Blood was obtained before and 15 and 60 min after the infusion began. CRF significantly increased iACTH at 15 (younger group) and 60 min (both groups). CRF significantly increased bACTH and the bACTH-to-iACTH ratio (bACTH/iACTH) in both groups at 15 and 60 min. AVP significantly increased iACTH, bACTH, and bACTH/iACTH in both groups at 15 min. In two subgroups (n = 4/subgroup), CRF significantly increased ACTH-(1-39) and ACTH precursors at 15 and 60 min. CRF increased the ratio of ACTH-(1-39) to ACTH precursors [ACTH-(1-39)/ACTH precursors] at 15 (younger group) and 60 min (both groups). AVP increased ACTH-(1-39), ACTH precursors, and ACTH-(1-39)/ACTH precursors in both groups at 15 min. These findings show that both CRF and AVP can stimulate the secretion of bACTH, ACTH-(1-39), and ACTH precursors at 0.70 and 0.90 gestation. The proportional increments in bACTH/iACTH and ACTH-(1-39)/ACTH precursors suggest that CRF and AVP evoke selective increases in bACTH and ACTH-(1-39).

Regulation of ACTH secretory pathways in cultured pituitary cells

1991 ◽  
Vol 261 (5) ◽  
pp. C793-C798 ◽  
Author(s):  
J. Schwartz ◽  
S. Gibson ◽  
A. White
Keyword(s):  
Anterior Pituitary ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Receptor Complex ◽  
Response Mechanism ◽  
Acth Secretion ◽  
Secretory Pathways ◽  
Anterior Pituitary Cells ◽  
Acth Release

Although chloroquine, an agent that disrupts regulated protein secretion, has previously been shown to decrease the adrenocorticotropic hormone (ACTH) secretory response to adenosine 3',5'-cyclic monophosphate or corticotropin-releasing factor (CRF) in AtT-20 and rat anterior pituitary cells, respectively, it has no effect on the response to vasopressin. The present study extended experiments with chloroquine to cultured sheep anterior pituitary cells, which have a greater maximum response to vasopressin. Chloroquine (200 microM) had no effect on basal ACTH secretion or on stimulation by vasopressin. In contrast to the rat, the net response to CRF was tripled by chloroquine in ovine cells. The effect of chloroquine on the response to CRF was more effective by coexposure of cells to CRF and chloroquine than by pretreatment with chloroquine. Monensin or vinblastine did not increase the ACTH response to CRF. The results indicate ACTH release in response to vasopressin is chloroquine insensitive in this way, can be dissociated from the mechanism that responds to CRF, and would be consistent with the CRF response mechanism involving pathways that can alter the secretory pool of ACTH. When chloroquine acts to increase the response to CRF, it is likely not to act by stabilizing the CRF-receptor complex.

Steroid inhibition of canine ACTH: in vivo evidence for feedback at the corticotrope

1988 ◽  
Vol 255 (3) ◽  
pp. E241-E246 ◽  
Author(s):  
M. Keller-Wood ◽  
E. Leeman ◽  
J. Shinsako ◽  
M. F. Dallman
Keyword(s):  
Analysis Of Variance ◽  
Significant Interaction ◽  
Adrenocorticotropic Hormone ◽  
Delayed Feedback ◽  
Corticotropin Releasing Factor ◽  
Conscious Dogs ◽  
Acth Secretion ◽  
Glucocorticoid Treatment ◽  
Synthetic Steroids

We infused submaximal feedback doses of either dexamethasone (DEX; 0.1 microgram.kg-1.min-1) or corticosterone and cortisol (B+F; 1.5 micrograms.kg-1.min-1) intravenously for 40 min into conscious dogs and measured the adrenocorticotropic hormone (ACTH) responses to hypoglycemia induced by insulin (0.1 U/kg) or to ovine corticotropin-releasing factor (oCRF; 1 microgram/kg); both agents were injected at 120 min. The dose of DEX was chosen to produce suppression of the ACTH response to oCRF equivalent to that produced by B+F. The purpose of the study was to determine 1) whether CRF- and hypoglycemia-induced ACTH secretion are equally inhibited by glucocorticoid treatment and 2) whether DEX and B+F have differential effects in the inhibition of stress-induced ACTH secretion. We found that peak ACTH responses to hypoglycemia and CRF were equally inhibited by DEX (36 +/- 6 and 52 +/- 9%, respectively). The peak ACTH responses to hypoglycemia and CRF were also equally inhibited after B+F infusion (45 +/- 13 and 65 +/- 5%, respectively). There was no significant interaction between the steroid administered and the stimulus given in controlling the ACTH response (by 2-way analysis of variance). The results suggest that pituitary feedback is of primary importance in suppression of canine ACTH secretion by delayed feedback and that the natural and synthetic steroids both act at this site.

Cyproheptadine-Induced Remission of Cushing's Disease Due to Pituitary Basophil Adenoma

1982 ◽  
Vol 16 (12) ◽  
pp. 962-965 ◽  
Author(s):  
J. Jimenez-Alonso ◽  
J. Munoz-Avila ◽  
L. Jaimez ◽  
F. Pérez-Jimenez ◽  
C. Bellido ◽  
...  
Keyword(s):  
Cushing’S Disease ◽  
Pituitary Tumors ◽  
Corticotropin Releasing Factor ◽  
Cushing's Disease ◽  
Patient Support ◽  
Acth Secretion ◽  
Hypothalamic Regulation ◽  
Potent Antagonist ◽  
Factor Secretion ◽  
Acth Release

Serotonin is involved in the control of ACTH secretion, possibly by stimulating corticotropin releasing factor secretion from the hypothalamus. Cushing's disease seems to be due to defective hypothalamic regulation of ACTH release from the pituitary gland. Cyproheptadine is a potent antagonist of serotonin and has been used successfully in some patients with Cushing's disease, although, generally, in women without radiological evidence of pituitary tumors. We report the successful use of cyproheptadine in a 54-year-old man with Cushing's disease due to pituitary basophil adenoma. Significant clinical and biochemical improvement was noted 45 days after treatment began. The results in this patient support our findings that cyproheptadine can be effective in patients with Cushing's disease due to pituitary tumors, as well as in preparing very ill patients for surgery or managing such patients until radiotherapy takes effect.

Synthetic competitive antagonists of corticotropin-releasing factor: effect on ACTH secretion in the rat

Science ◽  
1984 ◽  
Vol 224 (4651) ◽  
pp. 889-891 ◽  
Author(s):  
J Rivier ◽  
C Rivier ◽  
W Vale
Keyword(s):  
Corticotropin Releasing Factor ◽  
Acth Secretion ◽  
Factor Effect

Corticotropin-releasing factor in the ovine fetus and pregnant ewe: role of placenta

1991 ◽  
Vol 261 (4) ◽  
pp. R995-R1002 ◽  
Author(s):  
M. Keller-Wood ◽  
C. E. Wood
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Late Pregnancy ◽  
Maternal Plasma ◽  
Corticotropin Releasing Factor ◽  
Late Gestation ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Arterial Plasma ◽  
Pregnant Ewe

In the sheep, maternal plasma adrenocorticotropic hormone and cortisol are increased in late pregnancy, and fetal plasma cortisol and adrenocorticotropic hormone rise precipitously in late gestation. To test whether the ovine placenta secretes corticotropin-releasing factor (CRF) into either the maternal or fetal circulation, pregnant ewes and their fetuses were prepared with femoral arterial catheters and uterine and umbilical venous catheters. Samples were taken from all sites before and during hypoxia. There was no difference in CRF concentration across the placenta in the mothers or the fetuses under resting or hypoxemic conditions, but maternal and fetal arterial plasma CRF concentrations increased between 128 and 145 days. In a second study, maternal and fetal femoral venous plasma CRF concentrations were measured 1-19 days before spontaneous parturition. The mean concentration increased 8.6 +/- 0.6 pg/ml 11-19 days before parturition to 13.0 +/- 1.0 and 13.2 +/- 1.4 pg/ml in fetuses 4-8 and 1-3 days before parturition, respectively. Maternal plasma concentrations did not significantly increase in the days closer to parturition. These studies demonstrate that there are low but measurable CRF concentrations in fetal and maternal sheep plasma but that these are not the result of tonic placental secretion of CRF.

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