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.

A COMPARISON OF THE EFFECTS OF FOUR ERGOT DERIVATIVES ON PROLACTIN SECRETION BY DISPERSED RAT PITUITARY CELLS

1980 ◽  
Vol 87 (1) ◽  
pp. 95-103 ◽  
Author(s):  
G. DELITALA ◽  
T. YEO ◽  
ASHLEY GROSSMAN ◽  
N. R. HATHWAY ◽  
G. M. BESSER
Keyword(s):  
Anterior Pituitary ◽  
Ergot Alkaloids ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Inhibitory Effects ◽  
Prolactin Release ◽  
Ergot Derivatives ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

The inhibitory effects of dopamine and various ergot alkaloids on prolactin secretion were studied using continuously perfused columns of dispersed rat anterior pituitary cells. Bromocriptine (5 nmol/l) and lisuride hydrogen maleate (5 nmol/l) both inhibited prolactin secretion, the effects persisting for more than 3 h after the end of the administration of the drugs. A similar although less long-lasting effect was observed with lergotrile (50 nmol/l) and the new ergoline derivative, pergolide (5 nmol/l). These effects contrasted with the rapid disappearance of the action of dopamine. The potency estimates of the ergots relative to that of dopamine were: lergotrile, 2·3; bromocriptine, 13; lisuride, 15; pergolide, 23. The dopamine-receptor blocking drugs, metoclopramide and haloperidol, antagonized the prolactin release-inhibiting activity of the compounds; bromocriptine and lisuride showed the highest resistance to this dopaminergic blockade. The results suggested that the direct effect of the ergot derivatives on dispersed pituitary cells was mediated through dopamine receptors and emphasized the long-lasting action of bromocriptine and lisuride in vitro.

Effect of selective serotonin agonists on basal, corticotrophin-releasing hormone- and vasopressin-induced ACTH release in vitro from rat pituitary cells

1993 ◽  
Vol 136 (3) ◽  
pp. 381-387 ◽  
Author(s):  
A. E. Calogero ◽  
G. Bagdy ◽  
M. L. Moncada ◽  
R. D'Agata
Keyword(s):  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Receptor Subtype ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Level 2 ◽  
Acth Release

ABSTRACT The present study was undertaken to evaluate the serotonin (5-HT) receptor subtype(s) by which 5-HT acts on the pituitary to stimulate ACTH secretion. We tested the effects of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), the 5-HT1C receptor agonist metachloro-phenylpiperazine (m-CPP), which also binds to other 5-HT receptors with lower affinity, and the 5-HT2/1C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on basal, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP)-stimulated ACTH release from primary rat anterior pituitary cell cultures. 5-HT, 8-OH-DPAT and DOI significantly increased basal ACTH release, an effect which was antagonized by 5-HT receptor antagonists. 5-HT and DOI were effective at nanomolar concentrations whereas 8-OH-DPAT was effective at higher concentrations. 5-HT, 8-OH-DPAT (both at 10 nmol/l) and DOI (at higher concentrations) blunted the stimulatory effect of CRH. The suppressive effects of 8-OH-DPAT and DOI on CRH-stimulated ACTH release were antagonized by (−)propranolol, a β-adrenergic receptor antagonist which binds the 5-HT1A receptor with elevated affinity, and ketanserin, a 5-HT2 receptor antagonist respectively. 5-HT, 8-OH-DPAT and DOI showed additive stimulatory effects with AVP but only at the highest concentration tested, whereas m-CPP potentiated AVP-induced ACTH release at concentrations of 1 nmol/l or more. This effect was antagonized by metergoline, a non-selective 5-HT receptor antagonist and mianserin, an antagonist which binds the 5-HT1C receptor with elevated affinity. Thus (1) 5-HT and selective 5-HT agonists such as 8-OH-DPAT, m-CPP and DOI modulate ACTH release by acting directly at the pituitary level; (2) serotonergic stimulation of basal ACTH release is mediated by both 5-HT2 and 5-HT1A receptors; (3) serotonergic inhibition of CRH-stimulated ACTH release is mediated by 5-HT1A and 5-HT2 receptors; whereas (4) serotonergic potentiation of AVP-stimulated ACTH release is mediated mainly by 5-HT1C receptors. Journal of Endocrinology (1993) 136, 381–387

Isolated pituitary cells: glucocorticoids do not rapidly suppress ACTH secretion in response to CRF

1989 ◽  
Vol 256 (1) ◽  
pp. E145-E151 ◽  
Author(s):  
M. Familari ◽  
J. W. Funder
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Suppressive Effect ◽  
Inhibitory Response ◽  
Pituitary Cells ◽  
Concomitant Treatment ◽  
Inhibitory Effects ◽  
Acth Secretion ◽  
Acth Release

The possibility of a direct rapid suppressive effect of glucocorticoids on stimulated adrenocorticotropic hormone (ACTH) release was investigated in perifused normal pituitary cells attached to microcarriers. Forty-eight hours after attachment to Cytodex beads, cells were transferred to two columns (one experimental, one control), perifused at a rate of 300-350 microliters/min, and equilibrated for 3 h. Either rat or ovine corticotropin-releasing factor (CRF; 2 nM) were used to stimulate ACTH release, and fractions collected every 5 min were assayed for immunoreactive ACTH. Concomitant treatment with CRF and glucocorticoids (dexamethasone 100 nM or corticosterone 1 microM), or glucocorticoid pretreatment for up to 2 h, did not affect the release of ACTH occasioned by repetitive 5-min exposures to CRF at 30-min intervals. In addition, when ovine CRF was given as two 30-min infusions 1 h apart, neither concomitant steroid administration nor steroid pretreatment for 90 min affected the release of ACTH compared with controls. The lack of rapid steroid inhibition was not an artifact of enzymatic dispersion or microcarrier attachment, since no rapid inhibitory response was seen with acutely perifused rat anterior pituitary quarters. We thus conclude that in vitro rapid inhibitory effects of glucocorticoids on ACTH release do not occur at the level of the pituitary. Accordingly such action in vivo presumably reflects acute steroid-induced effects on the hypothalamus or higher centers.

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.

Effects of a novel 21-amino steroid, U74006F, on the rat pituitary-adrenocortical axis

1990 ◽  
Vol 126 (2) ◽  
pp. 203-209 ◽  
Author(s):  
J. M. Burrin ◽  
G. R. Hart
Keyword(s):  
Lipid Peroxidation ◽  
Chronic Administration ◽  
Pituitary Cells ◽  
Acth Secretion ◽  
Short Term ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Adrenalectomized Rats

ABSTRACT The 21-amino steroid U74006F is a potent inhibitor of lipid peroxidation and has been shown to affect beneficially the acutely injured central nervous system. Therapeutically, it is desirable for this compound to be devoid of steroid side-effects. We have demonstrated a significant (P < 0·001) inhibition of basal ACTH secretion from cultured rat pituitary cells during a 24-h incubation at concentrations (10–100 μmol/l) previously demonstrated to inhibit lipid peroxidation in vitro. U74006F also inhibited corticotrophin-releasing factor (CRF)-stimulated ACTH secretion significantly and the combination of dexamethasone and U74006F completely blocked CRF-41-stimulated ACTH secretion. Administration of U74006F in vivo (30 mg/kg, orally, every 6 h for 30 h) had no effect on ACTH levels in normal rats (84±38 vs 45±6 ng/l in control animals) but increased ACTH levels in adrenalectomized rats (1330±295 vs 464±79 ng/l in control animals, P < 0·02). This increase in ACTH was not observed when adrenalectomized animals were maintained on the same regime of U74006F for 5 days. Our data suggest that U74006F is capable of exerting inhibitory effects on ACTH secretion in vitro. In vivo, effects on ACTH secretion were stimulatory rather than inhibitory and only occurred short-term in adrenalectomized animals or chronically in adrenalectomized rats maintained on dexamethasone. No effects on the pituitary-adrenocortical axis were seen following short-term or chronic administration of U74006F in normal rats. Journal of Endocrinology (1990) 126, 203–209

Interleukin 6 possibly induced by interleukin 1β in the pituitary gland stimulates the release of gonadotropins and prolactin

1990 ◽  
Vol 122 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Masaaki Yamaguchi ◽  
Noboru Matsuzaki ◽  
Kenji Hirota ◽  
Akira Miyake ◽  
Osamu Tanizawa
Keyword(s):  
Pituitary Gland ◽  
Interleukin 6 ◽  
Anterior Pituitary ◽  
Interleukin 1 ◽  
Interleukin 1Β ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

Abstract The abilities of recombinant human interleukin 1 (IL-1) and IL-6 to induce release of FSH, LH and PRL from rat pituitary cells in vitro were examined. IL-1 and IL-6 induced significant releases of FSH, LH and PRL within 3 h. The extents of release of these compounds induced by IL-1 and IL-6 were similar to those induced by GnRH and TRH. Rat anterior pituitary cells released IL-6 spontaneously, and its release was enhanced by IL-1β. This effect of IL-1β was inhibited significantly by a rabbit anti-IL-1β antiserum. These findings suggest that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL-6 stimulated the secretions of FSH, LH and PRL.

Modulation of prolactin secretion by contraceptive progestins in cultured rat pituitary cells in vitro

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S188-S189
Author(s):  
L. KIESEL ◽  
T. RABE ◽  
D. SCHOLZ ◽  
V. KIRSCHNER ◽  
B. RUNNEBAUM
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

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

In vitro evidence of a role for inhibin in female rabbits

1984 ◽  
Vol 246 (3) ◽  
pp. E243-E248
Author(s):  
A. L. Goodman
Keyword(s):  
Granulosa Cells ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
C Cells ◽  
Rat Pituitary ◽  
Reference Preparation ◽  
Lh Release ◽  
Rat Pituitary Cells ◽  
I Cells

To examine a regulatory role for inhibin in female rabbits, an in vitro bioassay for inhibin activity was modified to use cultured rabbit pituitary cells and charcoal-extracted porcine follicular fluid (pFFx) as a reference preparation. pFFx inhibited follicle-stimulating hormone (FSH) release in a dose-dependent manner in cultures from both intact (I) and castrate (C) does at doses that also inhibited FSH release by cultured rat pituitary cells. Basal FSH release by I cells was inhibited greater than 10% by 0.02% (vol/vol) and greater than 90% by greater than or equal to 0.2% pFFx, whereas in C cells maximal inhibition of FSH release plateaued at only approximately 75%. FSH secretion was restored after removal of pFFx in day 2 media. Luteinizing hormone (LH) release by C cells was not inhibited at any dose of pFFx, but in I cells LH was progressively inhibited to approximately 60% of control levels during day 2 (but not day 1). Charcoal-extracted media (0.25-1%) in which 5 X 10(5) rabbit granulosa cells had been earlier cultured for 72 h produced a parallel inhibition of FSH release. The present findings demonstrate that 1) rabbit pituitary cells are responsive to inhibin, i.e., pFFx preferentially inhibited FSH secretion in a direct, graded, and reversible manner and 2) rabbit follicular granulosa cells secrete an inhibin-like substance.

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