ACTH responses to hypotension and feedback inhibition of ACTH increased by chronic progesterone treatment

1998 ◽  
Vol 274 (1) ◽  
pp. R81-R87
Author(s):  
Maureen Keller-Wood
Keyword(s):  
Arterial Pressure ◽  
Acute Treatment ◽  
Adrenocorticotropic Hormone ◽  
Feedback Inhibition ◽  
Acth Secretion ◽  
Baroreceptor Sensitivity ◽  
Feedback Effects ◽  
Plasma Progesterone ◽  
Progesterone Treatment ◽  
Simple Effect

During pregnancy, arterial pressure, baroreceptor sensitivity, and adrenocorticotropic hormone (ACTH) responses to hypotension are decreased. Basal ACTH and cortisol are increased in pregnancy, suggesting a reduction in cortisol feedback inhibition of ACTH. Acute treatment with progesterone decreases arterial pressure, baroreflex-mediated responses, and corticosteroid feedback effects on ACTH. These experiments test the hypothesis that chronic increases in progesterone produce changes in arterial pressure, ACTH responses to stress, and feedback inhibition of ACTH similar to pregnancy. Ewes were treated with progesterone for 60–80 days. This increase in plasma progesterone (to 7.6 ± 0.4 ng/ml) did not alter basal ACTH, cortisol, arterial pressure, or heart rate. However, ACTH and AVP responses to hypotension were augmented in progesterone-treated ewes compared with untreated ewes. Chronic progesterone treatment resulted in greater inhibition of ACTH by cortisol. Because chronic progesterone treatment did not decrease the ACTH response to hypotension or attenuate the feedback control of ACTH secretion, these results suggest that the changes in pituitary-adrenal control during pregnancy do not reflect a simple effect of progesterone alone.

NEGATIVE, RATE-SENSITIVE FEEDBACK EFFECTS ON ADRENOCORTICOTROPHIN SECRETION BY CORTISOL IN NORMAL SUBJECTS

1982 ◽  
Vol 92 (3) ◽  
pp. 443-448 ◽  
Author(s):  
S. C. J. READER ◽  
J. ALAGHBAND-ZADEH ◽  
J. R. DALY ◽  
W. R. ROBERTSON
Keyword(s):  
Negative Feedback ◽  
Feedback Inhibition ◽  
Fast Rate ◽  
Normal Subjects ◽  
Constant Infusion ◽  
Stress Tests ◽  
Nacl Solution ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Feedback Effects

Plasma ACTH and corticosteroid levels were measured in normal subjects during constant infusion of either 0·9% (w/v) NaCl solution or cortisol, and during insulin-induced hypoglycaemia. During infusions of 0·9% NaCl solution the secretion of ACTH and corticosteroids was episodic. Fast, rate-sensitive, negative feedback inhibition of ACTH secretion was observed during cortisol infusions, when the corticosteroid levels were within the physiological range (200–750 nmol/l) and were rising at a rate of between 5 and 10 nmol/l per min for 30 min or longer. When plasma corticosteroid levels were in a steady state, the initial fast feedback effects were abolished and ACTH secretion resumed. However, this recovery of ACTH secretion was not seen when the corticosteroid levels were persistently above 800 nmol/l. It appears that corticosteroid-induced negative feedback in man may be both rate- and level-sensitive. During insulin stress tests ACTH secretion fell at a time when the plasma corticosteroid level was rising rapidly (> 5 nmol/l per min) despite persistent hypoglycaemia.

Pregnancy alters cortisol feedback inhibition of stimulated ACTH: studies in adrenalectomized ewes

2001 ◽  
Vol 280 (6) ◽  
pp. R1790-R1798 ◽  
Author(s):  
Maureen Keller-Wood ◽  
Charles E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Feedback Inhibition ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Feedback Effects ◽  
Low Concentrations ◽  
Pregnancy And Postpartum ◽  
Cortisol Levels

These studies test the hypothesis that pregnancy alters the feedback effects of cortisol on stimulated ACTH secretion. Ewes were sham-operated (Sham), or adrenalectomized (ADX) at ∼108 days gestation and replaced with aldosterone (3 μg · kg−1· day−1) and with cortisol at either of two doses (ADX + 0.6 and ADX + 1 mg · kg−1· day−1); ewes were studied during pregnancy and postpartum. Mean cortisol levels produced in ADX ewes were similar to normal pregnant ewes (ADX+1) or nonpregnant ewes (ADX+0.6), respectively. Plasma ACTH concentrations in response to infusion of nitroprusside were significantly increased in the pregnant ADX+0.6 ewes (1,159 ± 258 pg/ml) relative to pregnant Sham ewes (461 ± 117 pg/ml) or the ADX+1 ewes (442 ± 215 pg/ml) or the same ewes postpartum (151 ± 69 pg/ml). Plasma ACTH concentrations were not significantly different among the groups postpartum. Increasing plasma cortisol to 20–30 ng/ml for 24 h before hypotension produced similar inhibition of ACTH in all groups. Pregnancy appears to decrease the effectiveness of low concentrations of cortisol to inhibit ACTH responses to hypotension.

Does intracarotid PGE2 increase plasma ACTH concentration in conscious adult ewes?

1991 ◽  
Vol 261 (3) ◽  
pp. E395-E401
Author(s):  
T. A. Cudd ◽  
C. E. Wood
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Human Contact ◽  
Acth Concentration

The hypothesis that prostaglandin E2 (PGE2) is a circulating mediator of adrenocorticotropic hormone (ACTH) secretion in sheep was tested in conscious adult ewes using 30-min carotid artery infusions of 0, 5, 10, 100, and 500 ng.kg-1. min-1 PGE2 in saline. ACTH, cortisol, and aldosterone were significantly increased during the 500 ng.kg-1.min-1 infusion (166 +/- 61 to 233 +/- 38 pg/ml, 27 +/- 5 to 45 +/- 2 ng/ml, and 52 +/- 11 to 85 +/- 25 pg/ml, respectively). PGE2 infusions of 100 ng.kg-1.min-1 increased ACTH from 104 +/- 31 to 168 +/- 31 pg/ml and cortisol from 18 +/- 5 to 42 +/- 2 ng/ml. PGE2 infusions did not increase arginine vasopressin, plasma renin activity, or hematocrit. Heart rate and mean arterial pressure were minimally but significantly increased during the 500 ng.kg-1.min-1 infusion, from 84.9 +/- 2.8 to 99.3 +/- 5.4 beats/min and 95.5 +/- 1.8 to 101.0 +/- 3.4 mmHg, respectively. In a second study to test whether lower infusion rates of PGE2 increase plasma ACTH in sheep with lower resting hormone concentrations, sheep were infused and sampled through a tether system, preventing any disturbances due to human contact the day of an experiment. For all infusion rates ACTH baselines were less than or equal to 55 +/- 17 pg/ml, and cortisol baselines were less than or equal to 6 +/- 3 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Short-term stimulation and feedback inhibition of ACTH secretion does not result in dissociation between cortisol and dehydroepiandrosterone secretion in man

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S60-S61
Author(s):  
T. H. SCHÜRMERYER ◽  
G. WILL ◽  
M. EICHNER ◽  
A. VON ZUR MÜHLEN
Keyword(s):  
Feedback Inhibition ◽  
Acth Secretion ◽  
Short Term

Early glucocorticoid feedback in anterior pituitary corticotrophs: differential inhibition of hormone release induced by vasopressin and corticotrophin-releasing factor in vitro

1991 ◽  
Vol 129 (2) ◽  
pp. 261-268 ◽  
Author(s):  
M. J. Shipston ◽  
F. A. Antoni
Keyword(s):  
Anterior Pituitary ◽  
Actinomycin D ◽  
Feedback Inhibition ◽  
Female Rats ◽  
Hormone Release ◽  
Type Ii ◽  
Acth Secretion ◽  
Corticotrophin Releasing Factor ◽  
Acth Release

ABSTRACT Vasopressin and 41-residue corticotrophin-releasing factor (CRF-41) are physiological mediators of the hypothalamic control of pituitary ACTH secretion, whilst adrenocortical glucocorticoids are the major inhibitory factors regulating ACTH output. In the present study it was investigated in vitro whether the characteristics of early glucocorticoid inhibition of stimulated ACTH secretion would differ depending on the nature of the stimulus and the temporal relationship between secretagogue and steroid. The experiments were carried out using perifused segments of rat adenohypophysis obtained from randomly cycling female rats. Repeated pulses (5 min) of CRF-41 or vasopressin were given at 1-h intervals for up to 7 h. The net release of ACTH became stable after the second secretagogue pulse. Administration of 0·1 μmol corticosterone/l 30 min before and during a 5-min pulse of 10 nmol CRF-41/l inhibited CRF-41-stimulated ACTH release to 60% of control. Stimulated hormone release remained suppressed at 90 min after the start of the corticosterone infusion and returned to control levels by 150 min. If corticosterone treatment (35 min total exposure) was started simultaneously with the CRF-41 pulse, no inhibitory effect of the steroid was observed at any subsequent time-point examined (60,90,120 and 150 min). In contrast, vasopressin-stimulated ACTH release was inhibited by approximately 50% when corticosterone was applied before, or simultaneously with, a 5-min pulse of 10 nmol vasopressin/l. The synthetic glucocorticoid type II receptor agonist RU28362, administered 30 min before and during a 5-min pulse of 10 nmol CRF-41/l, reduced CRF-41-stimulated ACTH release to 50% of control up to 2·5 h after the start of RU28362 application (although inhibition after 35 min exposure was not statistically significant). Inhibition of ACTH release stimulated by 10 nmol vasopressin/l was observed within 35 min of steroid application and was maintained up to 2·5 h after the initial application of RU28362. The action of RU28362 on CRF-41-stimulated ACTH release was blocked by inhibitors of transcription (actinomycin D) and translation (puromycin); notably these drugs did not modify the ACTH response to CRF-41. In contrast, actinomycin D as well as puromycin reduced vasopressin-stimulated ACTH release. The data suggest that: (1) the timing of steroid application is important in determining the early glucocorticoid inhibition of CRF-41- but not vasopressin-stimulated ACTH secretion; (2) CRF-41 and vasopressin mobilize different pools of ACTH from the anterior pituitary gland; (3) type II glucocorticoid receptors and synthesis of new protein(s) are involved in the early inhibitory action of glucocorticoids; (4) depending on the timing and nature of the incident secretagogue, differential negative feedback inhibition of ACTH secretion may occur at the pituitary level in vivo. Journal of Endocrinology (1991) 129, 261–268

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.

GONADAL HORMONES AND THE CONTROL OF OVULATION IN THE GUINEA-PIG

1972 ◽  
Vol 55 (3) ◽  
pp. 599-607 ◽  
Author(s):  
B. T. DONOVAN ◽  
A. N. LOCKHART
Keyword(s):  
Guinea Pig ◽  
Corpus Luteum ◽  
Acute Treatment ◽  
Gonadal Hormones ◽  
Time Of Day ◽  
Gonadal Steroids ◽  
Corpora Lutea ◽  
Plasma Progesterone ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate

SUMMARY The release of ovulating hormone after acute treatment with gonadal steroids, or corpus luteum removal on different days of the oestrous cycle, was studied in the guinea-pig. Injection of 25, 50 or 100 μg oestradiol or 2·5 mg progesterone on day 13 of the cycle had no effect upon gonadotrophin secretion as judged by follicular histology, but markedly altered the sizes of the corpora lutea of the previous ovulation. Treatment with oestradiol on day 14 did not elicit gonadotrophin secretion. However, administration of the same hormones to animals given 10 μg oestradiol benzoate 24 h earlier caused ovulation or follicular luteinization. Progesterone (2·5 mg) appeared least effective in stimulating gonadotrophin release; 25 μg oestradiol were more effective when given at 12.00 h than at 24.00 h but treatment with both hormones caused ovulation when given at either time of day. Luteal volumes were not affected. Removal of corpora lutea during the second half of the cycle advanced the time of expected ovulation to day 15 or earlier when the procedure was carried out on days 8 or 9, but not on days 10–13. It is concluded that 4–5 days must elapse between the fall in plasma progesterone level associated with corpus luteum regression and the release of ovulating hormone.

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).

scholarly journals Delayed effect of low progesterone concentrations on bovine uterine PGF(2alpha) secretion in the subsequent oestrous cycle

Reproduction ◽  
2001 ◽  
pp. 643-648 ◽  
Author(s):  
A Shaham-Albalancy ◽  
Y Folman ◽  
M Kaim ◽  
M Rosenberg ◽  
D Wolfenson
Keyword(s):  
Corpus Luteum ◽  
Luteal Phase ◽  
Oestrous Cycle ◽  
Delayed Effect ◽  
Plasma Progesterone ◽  
Progesterone Secretion ◽  
Progesterone Treatment ◽  
Late Luteal Phase ◽  
Subsequent Cycle ◽  
Concentration Curves

Low progesterone concentrations during the bovine oestrous cycle induce enhanced responsiveness to oxytocin challenge late in the luteal phase of the same cycle. The delayed effect of low progesterone concentrations during one oestrous cycle on uterine PGF(2alpha) secretion after oxytocin challenge on day 15 or 16 of the subsequent cycle was studied by measuring the concentrations of the major PGF(2alpha) metabolite (13,14-dihydro-15-keto PGF(2alpha); PGFM) in plasma. Two experiments were conducted, differing in the type of progesterone treatment and in the shape of the low progesterone concentration curves. In Expt 1, progesterone supplementation with intravaginal progesterone inserts, with or without an active corpus luteum, was used to obtain high, or low and constant plasma progesterone concentrations, respectively. In Expt 2, untreated cows, representing high progesterone treatment, were compared with cows that had low but increasing plasma progesterone concentrations that were achieved by manipulating endogenous progesterone secretion of the corpus luteum. Neither experiment revealed any differences in plasma progesterone concentrations between the high and low progesterone groups in the subsequent oestrous cycle. In both experiments, both groups had similar basal concentrations of PGFM on day 15 (Expt 1) or 16 (Expt 2) of the subsequent oestrous cycle, 18 days after progesterone treatments had ended. In both experiments, the increases in PGFM concentrations in the low progesterone groups after an oxytocin challenge were markedly higher than in the high progesterone groups. These results indicate that low progesterone concentrations during an oestrous cycle have a delayed stimulatory effect on uterine responsiveness to oxytocin during the late luteal phase of the subsequent cycle. This resulting increase in PGF(2alpha) secretion may interfere with luteal maintenance during the early stages of pregnancy.

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