THE RELEASE OF CORTICOTROPHIN BY ANTERIOR PITUITARY TISSUE IN VITRO

The release of ACTH by rat anterior pituitary tissue in vitro was used as a test system for the detection of factors that stimulate ACTH-release. The results indicate that:1. Epinephrine or arterenol, added by themselves, are without effect.2. Hypothalamic tissue alone is also ineffective.3. The combination of hypothalamic tissue with epinephrine or arterenol increases the release of ACTH about threefold.4. Brain cortex can replace hypothalamus.5. Liver cannot replace neural tissue; acetyl choline and serotonin cannot replace epinephrine or arterenol.6. The greatest stimulation of ACTH-release (six- to eight-fold) occurs with posterior pituitary tissue plus arterenol. The arterenol may be replaced by hypothalamus or sphingosine, but not by dopamine (3,4-dihydroxyphenylethylamine), which is structurally similar to arterenol.7. The posterior pituitary is probably involved in the response of the anterior pituitary–adrenocortical system to stress.

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cAMP-dependent ACTH secretagogues facilitate corticotropin releasing activity of angiotensin II on rat anterior pituitary cells in vitro

Acta Endocrinologica ◽

10.1530/acta.0.1140118 ◽

1987 ◽

Vol 114 (1) ◽

pp. 118-123 ◽

Cited By ~ 1

Author(s):

P. Schoenenberg ◽

R. C. Gaillard ◽

P. Kehrer ◽

A. F. Muller

Keyword(s):

Angiotensin Ii ◽

Anterior Pituitary ◽

Fold Increase ◽

Pituitary Cells ◽

Camp Production ◽

Camp Pathway ◽

Anterior Pituitary Cells ◽

Stimulation Of ◽

Acth Release

Abstract. Both arginine vasopressin (AVP) and angiotensin II (All) potentiate the corticotropin-releasing activity of CRF41 via a potentiation of CRF41-induced cAMP production. In perfused rat anterior pituitary cells, AII (10−8 mol) showed a transitory 2-fold increase in its ACTH-releasing activity, when tested after application extract of rat stalk median eminence. In order to determine whether this facilitating effect on All corticotropin-releasing activity occurred through cAMP-dependent mechanisms, the ACTH-releasing activity of All was tested after stimulation with CRF41, AVP or forskolin, three secretagogues with known effects on cAMP production. When given 16 min after CRF41, 10 μg/l, All (10−8 mol) showed a significant increase (210%) in its ACTH-releasing activity, which returned to the normal level when All-stimulation was repeated at 32 min (121%) and 48 min (100%). Similarly, forskolin, 3 × 10−6 mol, produced a significant transitory increase (208%) in the subsequent All-induced ACTH release whereas AVP, 10 μg/l and 100 μg/l, had no effect on the following ACTH response to All. These results suggest that the All-induced ACTH secretion – which is cAMP independent – nevertheless may be modulated by previously stimulation of the cAMP pathway.

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INHIBITION BY CORTISOL OF ACTH RELEASE FROM ANTERIOR PITUITARY TISSUE IN VITRO

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y66-070 ◽

1966 ◽

Vol 44 (4) ◽

pp. 549-556 ◽

Cited By ~ 3

Author(s):

John J. Pollock ◽

Frank S. LaBella

Keyword(s):

Adrenal Cortex ◽

Incubation Medium ◽

Anterior Pituitary ◽

Pituitary Tissue ◽

Pituitary Glands ◽

Cortex Slices ◽

Acth Release

The central basophilic region of bovine anterior pituitary glands was incubated for 30 minutes with varying concentrations of cortisol. Dialyzed incubation medium was subsequently assayed for ACTH activity by measuring the increased production of steroids from bovine adrenal cortex slices. Inhibition of ACTH release was evident with 5.5 × 10−11 M cortisol, but was more pronounced and consistent with 5.5 × 10−8 M or higher. Concentrations of 5.5 × 10−6 and 5.5 × 10−5 M were generally less effective in causing inhibition of ACTH release than were concentrations of 5.5 × 10−8 and 5.5 × 10−7 M.

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Biosynthesis of growth hormone in the rat anterior pituitary gland. Stimulation of biosynthesis in vitro by insulin

Biochemical Journal ◽

10.1042/bj1341103 ◽

1973 ◽

Vol 134 (4) ◽

pp. 1103-1113 ◽

Cited By ~ 1

Author(s):

A. Betteridge ◽

M. Wallis

Keyword(s):

Growth Hormone ◽

Anterior Pituitary ◽

Rna Synthesis ◽

Glucose Utilization ◽

Actinomycin D ◽

Hormone Synthesis ◽

Pituitary Glands ◽

Hormone Biosynthesis ◽

Stimulation Of

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.

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

Journal of Endocrinology ◽

10.1677/joe.0.1290261 ◽

1991 ◽

Vol 129 (2) ◽

pp. 261-268 ◽

Cited By ~ 14

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

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Bovine Posterior Pituitary Extract Stimulates Prolactin Release from the Anterior Pituitary Gland In Vitro and In Vivo in Cattle

Reproduction in Domestic Animals ◽

10.1111/j.1439-0531.2005.00580.x ◽

2005 ◽

Vol 40 (2) ◽

pp. 184-189 ◽

Cited By ~ 16

Author(s):

T Hashizume ◽

T Sasaki ◽

S Nonaka ◽

T Hayashi ◽

M Takisawa ◽

...

Keyword(s):

Pituitary Gland ◽

Anterior Pituitary ◽

Anterior Pituitary Gland ◽

Posterior Pituitary ◽

Pituitary Extract ◽

Prolactin Release

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Evidence for a role of phospholipase A2 in the mechanism of LHRH priming in rat anterior pituitary tissue

Journal of Endocrinology ◽

10.1677/joe.0.1410015 ◽

1994 ◽

Vol 141 (1) ◽

pp. 15-31 ◽

Cited By ~ 5

Author(s):

F J Thomson ◽

M S Johnson ◽

R Mitchell ◽

B Wolbers

Keyword(s):

Protein Synthesis ◽

Anterior Pituitary ◽

Priming Effect ◽

Protein Synthesis Inhibitor ◽

Synthesis Inhibitor ◽

Pituitary Tissue ◽

Gonadotrophin Secretion ◽

Lh Release ◽

Functional Relevance

Abstract The phospholipase A2 (PLA2) inhibitors, quinacrine, p-bromophenacyl bromide, ONO-RS-082, aristolochic acid and chloracysine blocked the priming effect of LHRH, but not acute LHRH-induced gonadotrophin release measured in anterior pituitary pieces in pro-oestrous rats in vitro. These results suggest that the intracellular mechanisms underlying LHRH priming are distinct from those which mediate LH release in the present circumstances in that they involve PLA2. Furthermore, neither LHRH-induced LH release from preprimed tissue nor Ca2+-induced LH release were attenuated by quinacrine, indicating that this inhibitor does not interfere with the general Ca2+-dependent secretory apparatus of the gonadotroph and that the critical period for its action is in the induction of priming. LHRH induced the release of [3H]arachidonic acid ([3H]AA) from [3H]AA-prelabelled anterior pituitary tissue from pro-oestrous rats; a response which was sensitive to inhibitors of PLA2, of protein kinase C (PKC) and of protein synthesis. Activation of PKC also resulted in [3H]AA release which was inhibited with exactly the same pharmacological profile as the response to LHRH. Both gonadotrophin secretion and [3H]AA release responses to LHRH and to phorbol ester varied in parallel during the oestrous cycle and in ovariectomized/oestradiol-17β-replaced animals, as did their sensitivity to quinacrine and the protein synthesis inhibitor cycloheximide. These results indicate that LHRH priming is dependent on a hormonally regulated cascade involving a distinct form of PKC acting through a protein synthesis-dependent step to release AA by means of PLA2 activity. The priming effect was mimicked (at least in part) by conditioning preincubation with AA, confirming the functional relevance of this signalling cascade. Results using standard inhibitors of lipoxygenase/epoxygenase pathways were equivocal as to whether these pathways were critically involved, whilst cyclo-oxygenase inhibitors were completely without effect. The steps downstream from AA (and its possible metabolites) by which stimulus–secretion coupling is up-regulated in priming remain to be clarified. Journal of Endocrinology (1994) 141, 15–31

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Evidence for a thyroid-inhibiting factor of adenohypophysial origin

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1964.206.5.1145 ◽

1964 ◽

Vol 206 (5) ◽

pp. 1145-1150 ◽

Cited By ~ 1

Author(s):

Israel Posner ◽

Enrique Pimentel

Keyword(s):

Anterior Pituitary ◽

Inhibitory Effect ◽

In Vivo Studies ◽

Pituitary Extract ◽

Inhibiting Factor ◽

Rat Thyroid ◽

Tsh Stimulation ◽

Stimulation Of

Thyroids of normal or thyroxine ( T4)-pretreated rats were incubated in vitro in a serum medium containing I131. It was found that the addition of either a whole rat adenohypophysis, a crude rat anterior pituitary extract, or of commercial bovine thyrotrophin (TSH) to the medium caused a slight stimulation of I131 release and no apparent stimulation but rather an immediate and considerable inhibition of thyroid-I131 uptake. Preincubation of rat thyroid with crude anterior pituitary extract resulted in a prolonged inhibitory effect on the thyroid-I131 uptake. In vivo studies showed that shortly after TSH administration a similar inhibition of uptake occurred in normal rats, although allowing 24 hr for TSH stimulation brought about no change in iodine uptake in thyroids of normal and a marked increase in uptake by thyroids of T4-pretreated rats. The inhibition of thyroid-I131 uptake was assumed to have been caused either by TSH itself, or by a thyroid-inhibiting factor of adenohypophysial origin present in commercial TSH preparations as a contaminant.

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