ACTH secretion from isolated hypophysial anterior lobes of male and female newborn rats: effects of corticotrophin-releasing factor, arginine vasopressin and oxytocin alone or in combination

1993 ◽  
Vol 137 (1) ◽  
pp. 123-132 ◽  
Author(s):  
L. Hary ◽  
J. P. Dupouy ◽  
A. Chatelain
Keyword(s):  
Arginine Vasopressin ◽  
Anterior Pituitary ◽  
Newborn Rats ◽  
Acth Secretion ◽  
Peripheral Plasma ◽  
Corticotrophin Releasing Factor ◽  
Males And Females ◽  
Dose Dependent ◽  
Acth Release

ABSTRACT ACTH release by the anterior pituitary lobes of 8-day-old newborn rats (males and females) in the presence of rat corticotrophin-releasing factor (rCRF), arginine vasopressin (AVP) and oxytocin, given alone or in association, was measured in vitro. Rat CRF and AVP induced a dose-dependent release of ACTH in both sexes, while oxytocin was unable to stimulate ACTH secretion except at the highest dose tested. No sex-related difference was noted for any of the responses. Oxytocin (1 nmol/l) potentiated the response to rCRF (0·20 nmol/l) by the anterior pituitary lobes of females but not by those of males. This oxytocin potentiation was abolished when female newborn rats were injected at birth with testosterone (1 mg). AVP (1 nmol/l) alone stimulated ACTH release from the anterior pituitary lobes of the newborn rats of both sexes and markedly potentiated the ACTH response to rCRF. Although no difference between the sexes was noted for basal levels of AVP and oxytocin in the hypothalamus, the neurointermediate lobe and the peripheral plasma, the present data on the sex-related effect of oxytocin on the newborn adenohypophysis could, in part, explain why ACTH release in response to ether stress was previously reported to be more lasting in females than in males on day 8 postpartum. Journal of Endocrinology (1993) 137, 123–132

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

Effect of acetylcholine and 5-hydroxytryptamine on the secretion of corticotrophin-releasing factor-41 and arginine vasopressin from the rat hypothalamus in vitro

1989 ◽  
Vol 122 (3) ◽  
pp. 713-718 ◽  
Author(s):  
E. W. Hillhouse ◽  
N. G. N. Milton
Keyword(s):  
Arginine Vasopressin ◽  
Bioactive Substances ◽  
Rat Hypothalamus ◽  
Corticotrophin Releasing Factor ◽  
Dose Dependent ◽  
Isolated Rat ◽  
Stimulation Of

ABSTRACT Previous studies using the isolated rat hypothalamus in vitro have shown that both acetylcholine and 5-hydroxytryptamine (5-HT) stimulate the secretion of bioactive corticotrophin-releasing factor (CRF). However, the CRF complex consists of a number of bioactive substances, and in this study we examined the effect of acetylcholine and 5-HT on the release of immunoreactive (ir)-CRF-41 and ir-arginine vasopressin (AVP) in vitro. Acetylcholine caused a dose-dependent (10 pmol–10 nmol/l) release of both neuropeptides, and the effect was partially antagonized by both atropine and hexamethonium. Nicotine (0·1–10 μmol/l) also stimulated the release of both peptides, whereas bethanacol had no effect on AVP release, but had a variable action on CRF-41 release. 5-HT caused a dose-dependent (10 pmol–1 nmol/l) stimulation of CRF-41 release without any effect on AVP release, and this effect was antagonized by cyproheptadine, suggesting the participation of specific 5-HT receptors. Journal of Endocrinology (1989) 122, 713–718

RAT MELANIN CONCENTRATING HORMONE DOES NOT MODIFY THE RELEASE OF CRH-41 FROM RAT HYPOTHALAMUS OR ACTH FROM THE ANTERIOR PITUITARY IN VITRO

1990 ◽  
Vol 127 (1) ◽  
pp. R1-R4 ◽  
Author(s):  
P. Navarra ◽  
S. Tsagarakis ◽  
D. H. Coy ◽  
L.H. Rees ◽  
G. M. Besser ◽  
...  
Keyword(s):  
Inhibitory Activity ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Inhibitory Effects ◽  
Acth Secretion ◽  
Rat Pituitary ◽  
Melanin Concentrating Hormone ◽  
Rat Pituitary Cells ◽  
Acth Release

ABSTRACT It has been suggested that melanin concentrating hormone (MCH) possesses potent corticotrophin (ACTH) inhibitory activity, on the basis of the inhibitory effects displayed by salmon MCH on ACTH release from either trout or rat isolated pituitary fragments. Recently, rat MCH has been characterised, and this prompted us to investigate the putative inhibitory activity of synthetic rat MCH on basal and stimulated ACTH secretion from freshly-dispersed rat pituitary cells or incubated rat pituitary fragments, as well on KCl (28 mmol/l) or noradrenaline-evoked release of corticotrophin releasing hormone-41 (CRH-41) from rat hypothalamic explants in vitro. There were no effects of rat MCH on either CRH-41 or ACTH release in vitro.

CORTICOTROPHIN-RELEASING FACTOR - MEDIATED ADRENOCORTICOTROPHIN RELEASE FROM RAT ANTERIOR PITUITARY CELLS IS POTENTIATED BY C-TERMINAL GASTRIN-RELEASING PEPTIDE

1984 ◽  
Vol 102 (2) ◽  
pp. R1-R3 ◽  
Author(s):  
A.C. Hale ◽  
J. Price ◽  
J.F. Ackland ◽  
I. Doniach ◽  
S. Ratter ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
In Vitro Release ◽  
Surgical Removal ◽  
Pituitary Cells ◽  
Gastrin Releasing Peptide ◽  
Corticotrophin Releasing Factor ◽  
Anterior Pituitary Cells ◽  
Isolated Rat ◽  
Acth Release

ABSTRACT The remission of Cushing's syndrome following surgical removal of a tumour containing bombesin-like immunoreactivity (BLI), but insignificant levels of ACTH, is described. However, an acid extract of the tumour tissue caused the release of ACTH from isolated rat anterior pituitary cells in vitro. These observations led to an investigation of the effects of synthetic C-terminal gastrin-releasing peptide (GRP(14-27)) on ACTH release from isolated rat anterior pituitary cells. GRP(14-27) (10-1000 ng/ml) directly stimulated the release of ACTH in vitro, whereas lower doses (10-1000 pg/ml), ineffective themselves in eliciting ACTH release, potentiated the CRF-mediated in-vitro release of ACTH.

Hypothalamic peptide regulation of ACTH secretion from sheep pituitary

1993 ◽  
Vol 265 (4) ◽  
pp. R840-R845 ◽  
Author(s):  
R. J. Kemppainen ◽  
T. P. Clark ◽  
J. L. Sartin ◽  
C. A. Zerbe
Keyword(s):  
Angiotensin Ii ◽  
Anterior Pituitary ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Ang Ii ◽  
Acth Secretion ◽  
Low Concentrations ◽  
Acth Release

The relative abilities of the hypothalamic peptides corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT), and angiotensin II (ANG II) to stimulate adrenocorticotropic hormone (ACTH) secretion from cultured sheep anterior pituitary cells were studied. Incubation of cells with CRF, AVP, and OT, but not ANG II, was associated with increased ACTH secretion. CRF and AVP were equally effective in stimulating ACTH release at 0.1 nM, but larger doses of each resulted in distinctly different ACTH secretory patterns. The minimally effective dose of OT was 10 nM; greater doses of this peptide resulted in ACTH secretory responses similar to those measured after addition of AVP. Cotreatment with ANG II did not affect the ACTH-secretory response to CRF, AVP, or OT. These data confirm that AVP is a potent stimulus for ACTH secretion from sheep anterior pituitary in vitro and also show that CRF is effective in low concentrations in releasing ACTH. In contrast, the data do not support a regulatory role for ANG II in stimulating ACTH release directly from sheep corticotroph cells.

Vasopressin receptors influencing the secretion of ACTH by the rat adenohypophysis

1987 ◽  
Vol 113 (3) ◽  
pp. 389-396 ◽  
Author(s):  
J. C. Buckingham
Keyword(s):  
Receptor Antagonist ◽  
Arginine Vasopressin ◽  
Receptor Agonist ◽  
Intrinsic Activity ◽  
Corticotrophin Releasing Factor ◽  
Low Concentrations ◽  
Vasopressin Receptors ◽  
Acth Release

ABSTRACT The effects of selective agonists and antagonists of type 1 (V1) and type 2 (V2) vasopressin receptors on the secretion of ACTH in vitro by segments of adenohypophysial tissue and in vivo in rats pretreated with pentobarbitone and chlorpromazine were studied in the presence and absence of the 41 amino acid-containing peptide, corticotrophin-releasing factor-41 (CRF-41). The non-selective vasopressin receptor agonist, arginine vasopressin (AVP) and the V1-receptor agonist, felypressin caused dose-related increases in ACTH release in vivo and in vitro but the V2-receptor agonist, desmopressin was only weakly active in this respect. Their actions in vitro were antagonized competitively by the V1-receptor antagonist, d(C2H5)2-AVP, but were unaffected by the V2-receptor antagonist, d(CH2)5-d-Iso2-Thr4-AVP. Arginine vasopressin, felypressin and desmopressins in concentrations considerably lower than those necessary to elicit directly the release of ACTH, potentiated, in a dose-related manner, the activity of CRF-41 in vitro. The potentiating effects were not antagonized by the V2-receptor antagonist or by low concentrations of the V1 -receptor antagonist. At a higher concentration, the V1-receptor antagonist reduced, but did not abolish, the potentiating effects of AVP and its analogues. However, at this concentration, it also exhibited weak intrinsic activity and, like the agonists, potentiated the response to CRF-41. The results suggest that the direct effect of AVP on ACTH release is mediated by V1-like receptors. The vasopressin receptors involved in the potentiation of CRF-41 activity appear to be different. J. Endocr. (1987) 113, 389–396

Effect of noradrenaline and γ-aminobutyric acid on the secretion of corticotrophin-releasing factor-41 and arginine vasopressin from the rat hypothalamus in vitro

1989 ◽  
Vol 122 (3) ◽  
pp. 719-723 ◽  
Author(s):  
E. W. Hillhouse ◽  
N. G. N. Milton
Keyword(s):  
Arginine Vasopressin ◽  
Aminobutyric Acid ◽  
Basal Secretion ◽  
Acth Secretion ◽  
Rat Hypothalamus ◽  
Corticotrophin Releasing Factor

ABSTRACT Much controversy exists concerning the role of catecholamines in the control of ACTH secretion. In this study, noradrenaline (0·1 nmol–0·1 μmol/l) stimulated the release of both immunoreactive corticotrophin-releasing factor-41 (ir-CRF-41) and ir-arginine vasopressin (ir-AVP) from the rat hypothalamus in vitro. The stimulatory effect of noradrenaline on CRF-41 release was blocked by propranolol, whilst that on AVP release was blocked by phentolamine. γ-Aminobutyric acid (GABA; 10 nmol/l) inhibited the acetylcholine-induced release of both AVP and CRF-41 in vitro, and the effect was blocked by picrotoxin (0·1 μmol/l). Neither substance had any effect on the basal secretion of either neuropeptide. The results indicate that noradrenaline stimulates and GABA inhibits the release of both peptides from the rat hypothalamus in vitro. Journal of Endocrinology (1989) 122, 719–723

In-vitro effects of corticosterone, synthetic ovine corticotrophin releasing factor and arginine vasopressin on the release of adrenocorticotrophin by fetal rat pituitary glands

1984 ◽  
Vol 101 (3) ◽  
pp. 339-344 ◽  
Author(s):  
J. P. Dupouy ◽  
A. Chatelain
Keyword(s):  
Arginine Vasopressin ◽  
Fetal Life ◽  
Spontaneous Release ◽  
Sharp Rise ◽  
Corticotrophin Releasing Factor ◽  
Fetal Rat ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Acth Release

ABSTRACT The in-vitro release of ACTH by fetal rat pituitary glands on days 17, 19 and 21 of pregnancy was measured using radioimmunoassay. The spontaneous release of ACTH, expressed in pg ACTH/gland per h, increased with fetal age, in correlation with the sharp rise in pituitary ACTH content. However, since pituitary ACTH content was nearly sevenfold higher at term than on day 17, while basal release of ACTH was only threefold higher, one can speculate that the spontaneous release of ACTH was proportionally greater on day 17 than on day 21 of gestation. As corticosterone, at a physiological concentration (865 nmol/l), reduced ACTH release, it was concluded that the pituitary gland was one site of the negative feedback action of the corticosteroids during fetal life. Quantities of synthetic ovine corticotrophin releasing factor (CRF) which gave concentrations of 0·3–30 nmol/l in the incubation medium induced a sharp rise in ACTH release which was log-dose dependent between 0·3 and 3 nmolCRF/1 on day 17 and between 0·3 and 30 nmolCRF/1 on days 19 and 21. The response to CRF increased with fetal age. Quantities of arginine vasopressin (AVP) which gave concentrations of 2–200 nmol/l stimulated ACTH release at all stages of gestation investigated. However, the response to AVP was much lower than that to CRF. Potentiation of CRF-induced ACTH release was not observed when whole pituitary glands from 21-day-old fetuses were incubated with AVP (20 nmol/l) + CRF (3 nmol/l). Such results were correlated with the ontogenesis of immunoreactive vasopressin- and CRF-containing fibres in the median eminence of the rat fetus, as well as with the CRF-like immunoreactivity present in adult rat pituitary portal plasma and the AVP content of the fetal rat hypophysis. J. Endocr. (1984) 101, 339–344

The effects of corticotrophin-releasing hormone, arginine vasopressin and their antagonists on ACTH release from perifused horse anterior pituitary cells

1994 ◽  
Vol 143 (1) ◽  
pp. 85-93 ◽  
Author(s):  
M J Ellis ◽  
R S Mulligan ◽  
M J Evans ◽  
R A Donald
Keyword(s):  
Arginine Vasopressin ◽  
Anterior Pituitary ◽  
Dose Range ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
The Individual ◽  
Acth Release

Abstract Antagonists are useful for probing hormone action and receptor characteristics. In this study we have investigated the inhibitory effects of analogues of arginine vasopressin (AVP) and corticotrophin-releasing hormone (CRH) on stimulated release of immunoreactive ACTH from perifused equine anterior pituitary cells in vitro. Our aims were to gain some insight into the characteristics of the CRH and AVP receptors of the horse pituitary and to establish whether the response induced by AVP and CRH together could be blocked by combining antagonists. Experimental design included 5-min pulses of AVP (12·5 nmol/l), CRH (0·3 nmol/l) or CRH plus AVP given every 40 min alternately with pulses of secretagogue(s) plus appropriate antagonist(s). The effect of combined antagonists on the response to lower secretagogue concentrations (CRH, 0·03 nmol/l plus AVP, 2·5 nmol/l) was also tested. Response in the presence of an antagonist was compared with the mean response to secretagogue in the immediately preceding and following pulse and was expressed as per cent expected ACTH. The ACTH response to AVP was inhibited over the dose range 0·4–50 μmol/l by Phaa-d-Tyr(Et)2Lys6Arg3VP (P<0·002; ANOVA) and by d(CH2)5[Tyr(Me)2]AVP (P<0·001). Suppression of the expected ACTH response to AVP by these two antagonists was most effectively achieved by antagonist concentrations of 10 μmol/l (to 28±2·1%) and 25 μmol/l (to 22±5·1%) respectively. Inhibition was not improved by preinfusion compared with a bolus pulse. Aaa-d-Tyr(Et)2Val4Abu6Arg8·9VP and the non-peptide antagonist OPC-21268 had no inhibitory effect. Two α-helical (α-h) analogues of CRH, (α-hCRH(12–41) and α-hCRH(9–41) tested over the dose range 0·5–5 μmol/l, suppressed CRH-induced ACTH secretion (P<0·001) but CRH(23–41) had no significant effect. The α-hCRH(12–41) achieved greater suppression of ACTH release than the (9–41) derivative (8·7±4·2% compared with 19·3±3·5% of the expected ACTH response). Combination of d(CH2)5[Tyr(Me)2]AVP (25 μmol/l) plus α-hCRH (12–41) (5·0 μmol/l) achieved suppression to −0·5±1·3% and 0·8±1·5% of the expected response to CRH+AVP at 0·3+12·5 nmol/l and 0·03+2·5 nmol/l respectively. These effects were greater than seen by the individual antagonists alone. The antagonist effects suggest that the CRH and AVP receptors of the equine pituitary have similar properties to those from other species and are consistent with the pituitary AVP receptor being unlike the V2 receptor and resembling but not being identical to the V1 type. We also conclude that α-hCRH(12–41) and d(CH2)5[Tyr(Me)2]AVP can together block the ACTH response to CRH plus AVP and suggest that these antagonists should provide a means of investigating additional secretagogues involved in ACTH release in the horse. Journal of Endocrinology (1994) 143, 85–93

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