Roles of Intracellular and Extracellular Calcium in the Kinetic Profile of Adrenocorticotropin Secretion by Perifused Rat Anterior Pituitary Cells. I. Corticotropin Releasing Factor Stimulation*

Won, Justin G.S.; Orth, David N.

doi:10.1210/endo-126-2-849

Cited by 65 publications

(25 citation statements)

References 37 publications

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“…It is possible that TBP (bioactive fraction of the human plasma ultrafiltrate) contains factor(s) involved in the stress reaction or paracrine regulation of the growth factor synthesis, thus indirectly affecting the hormone release, but these possibilities have to be further evaluated. Finally, it is not impossible that TBP, like some other bioactive peptides (29)(30)(31)(32)(33)(34)(35), is involved in regulation of adenylate cyclase activity and/or calcium metabolism, thereby acting as a regulator of the hormonal activity of the normal and tumourous pituitary tissue.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the In Vitro Secretory Activity of Human Pituitary Adenomas: Modification of Corticotropin Release from Adenoma Tissue Explant Cultures by Addition of a Human Plasma Ultrafiltrate Bioactive Fraction

Žarković¹,

Hayn²,

Plavšić³

et al. 1996

CCLM

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Summary: The lack of control of tumour behaviour is manifested in different ways, depending primarily on the type of tumour. This results in numerous problems of tumour diagnosis and therapy. In the case of "benign" tumours, like pituitary adenomas, in vitro studies are often used for evaluation of the tumour. The use of tissue explant cultures of human pituitary adenomas and the comparison of the feature of cultured tumours with their behaviour in vivo showed that corticotropin is released not only from the tumours associated with Gushing^ disease, but also from clinically non-functioning tumours. Hence, it was supposed that the release of corticotropin in vivo from non-secreting tumours is probably under the influence of certain neuroendocrine and/or systemic humoral factors. To test this possibility, samples of 22 tumours were cultured in plain culture medium or in the presence of the "human plasma ultrafiltrate bioactive fraction" (tentatively termed as TBP) prepared by anion-exchange chromatography. In the presence of TBP the release of corticotropin was strongly inhibited in adenomas showing relatively high spontaneous secreting activity in vitro (> 200 ng/1 in 24 hours), while immunohistochemistry of these tumours indicated accumulation of corticotropin inside the cells. In contrast, TBP stimulated corticotropin release from tumours that showed relatively low basic corticotropin release (< 200 ng/1 in 24 hours), with no obvious change in cellular corticotropin immunoreactivity. Such a dual activity of TBP was not observed for 8 samples of adenomas cultured in the presence of surrounding pituitary tissue, probably because TBP did not affect corticotropin secretion by the normal pituitary cells (as indicated by immunohistochemistry). From these results, it appears that TBP could be one of the humoral factors involved in the regulation of corticotropin release from pituitary adenoma tissue. Its possible involvement in the regulation of corticotropin release from normal pituitary tissue, however, is uncertain.

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Section: Discussionmentioning

confidence: 99%

Analysis of the In Vitro Secretory Activity of Human Pituitary Adenomas: Modification of Corticotropin Release from Adenoma Tissue Explant Cultures by Addition of a Human Plasma Ultrafiltrate Bioactive Fraction

Žarković¹,

Hayn²,

Plavšić³

et al. 1996

CCLM

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“…Experimental evidence reported by different groups, that is secretion studies in the presence or absence of extracellular calcium or direct measurements of calcium transients in corticotropes exposed to OT or A VP (6,9,35,36), emphasizes the involvement of intracellular calcium stores during ACTH release. On the other hand, CRF causes influx of extracellular calcium through calcium channels, and these influxes are secondary to CRF-stimulated cAMP production (8,37,38). It has been proposed that calcium channels in a variety of cells are activated by cAMP (39,40).…”

Section: Discussionmentioning

confidence: 99%

“…In all cells analyzed, the OT-induced intracellular calcium transients were not substantially different when the steroids were present. (8,37,38). It has been proposed that calcium channels in a variety of cells are activated by CAMP (39,40).…”

Section: Glucocorticoidsmentioning

confidence: 99%

“…Therefore, we conclude that rapid inhibition of ACTH release by glucocorticoids interferes with cellular signal transduction beyond the step of calcium mobilization. (Endocrinology 132: [873][874][875][876][877][878]1993) the key role to trigger ACTH secretion (7)(8)(9). Indeed, studies with permeabilized ceIl preparations indicate that calcium is the main trigger substance in controlling exocytosis in exocrine (10,11) and endocrine cells (12)(13)(14)(15), including a corticotropic tumor cellline (16).…”

Section: Introductionmentioning

confidence: 99%

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Glucocorticoids rapidly inhibit oxytocin-stimulated adrenocorticotropin release from rat anterior pituitary cells, without modifying intracellular calcium transients

Link

1993

Endocrinology

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Glucocorticoid hormones suppress the secretion of ACTH evoked by secretagogues such as CRF and arginine vasopressin. In this study, we investigated the effects of glucocorticoids on ACTH release induced by oxytocin (OT) and on intracellular free calcium ion levels in corticotropes prepared from the adenohypophyses of female Wistar rats.Pulsatile additions of physiological concentration of OT (10 nM) to superfused anterior pituitary cells caused pulsatile ACTH release about 4-fold above basal secretion with similar peak amounts of ACTH du ring subsequent OT pulses. Exposure of the cells to corticosterone (100 nM) or to a selective glucocorticoid receptor agonist RU 28362 (100 nM) for 30 min suppressed OT-stimulated but not basal ACTH release by approximately 60%. Inhibition gradually disappeared during subsequent pulses of OT in the absence of corticosterone. Pretreatment with I

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“…CRH-mediated ACTH release strongly depends on the influx of extracellular calcium to the corticotrope via voltage-regulated calcium channels (21,22), and there is indeed some evidence to implicate such a step as defective in MD. First, there is increased calcium permeability in erythrocyte membranes from M D patients (23), and secondly, enhanced calcium influx through dystrophic hamster muscle cell membranes, under the influence of normal levels of parathormone has been observed (24).…”

Section: Discussionmentioning

confidence: 99%

Adrenocorticotropin Hyperresponsiveness in Myotonic Dystrophy Following Oral Fenfluramine Administration

Grice

Jackson

Penfold

et al. 1991

J Neuroendocrinology

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The plasma immunoreactive adrenocorticotropin and cortisol responses to oral fenfluramine hydrochloride (1.5 mglkg body wt) or placebo were examined in 11 patients with myotonic dystrophy, 4 controls with facioscapulohumeral dystrophy, a similarly debilitating muscle wasting disease, and 14 normal controls in single-blind studies performed in mid-afternoon.Mean areas under t h e adrenocorticotropin response versus time curve were significantly greater in myotonics (2573+429 pmol.min/L) than in facioscapulohumeral dystrophy controls (6961279 pmof.min/L, P < 0.02) and normals (560f 61 pmol.min/L, P < 0.0001). Corresponding cortisol responses were significantly greater in myotonics (35757 3949 nmol.min/L) than in normals (21828f 1669 nmol.min/L, P <0.001), but not significantly greater than those in facioscapulohumeral dystrophy controls (22830k6140 nmol.min/L, P = 0.055). No stressful side-effects which could affect hormone responses, and no significant changes in blood pressure or heart rate were noted. Fenfluramine activates central serotonergic and/or noradrenergic pathways initiating secretion of corticotropin-releasing hormone and possibly arginine vasopressin. W e postulate that these fenfluramine-activated pathways a r e hyperstimulated in myotonics, leading to adrenocorticotropin and cortisol hypersecretion. This may be a manifestation of a general cell membrane defect in myotonic dystrophy. W e found a lack of correlation of a g e (and severity of disease) with adrenocorticotropin response in myotonics, and therefore, the hyperresponse may serve as a useful marker for the disease before development of other overt signs.Myotonic dystrophy (MD) is a disorder of autosomal dominant inheritance, with the genetic locus on the long arm of chromosome 19 ( I ) . I t is thc most variable in clinical presentation of the muscular dystrophies, and no primary defect or generalized abnormality has yet been identified. In preliminary studies (2) we reported hypersecretion of adrenocorticotropin (ACTH) and 8-endorphin by myotonics compared to normal controls in response to exogenous ovine corticotropin-releasing hormone (CRH) and insulin-induced hypoglycaemia. Since C R H acts directly at the corticotrope ( 3 ) , and insulin-induced hypoglycaemia causes C R H release in man (4) and increased C R H mRNA levels in rats (5), we concluded that the ACTH hypersecretion in M D is due to a defect which is elicited by CRH-corticotrope interaction.To study the hypothalamic-pituitary-adrenal axis in M D further, we examined pituitary-adrenal responses to the ACTH secretagogue, fenfluramine (fen). Fen stimulates the hypothalamic-pituitary-adrenal axis (6-8) by an incompletely understood mechanism, generally considered to be mediated by serotonin (5-HT) (9), either by a hypothalamic action to release C R H (lo), or a direct effect, regarded as less important, of 5-HT on the anterior pituitary (1 1, 12). Another interpretation suggests that the ACTH-stimulating actions of fen, while ultimately effected by C R H and/or other sec...

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Roles of Intracellular and Extracellular Calcium in the Kinetic Profile of Adrenocorticotropin Secretion by Perifused Rat Anterior Pituitary Cells. I. Corticotropin Releasing Factor Stimulation*

Cited by 65 publications

References 37 publications

Analysis of the In Vitro Secretory Activity of Human Pituitary Adenomas: Modification of Corticotropin Release from Adenoma Tissue Explant Cultures by Addition of a Human Plasma Ultrafiltrate Bioactive Fraction

Analysis of the In Vitro Secretory Activity of Human Pituitary Adenomas: Modification of Corticotropin Release from Adenoma Tissue Explant Cultures by Addition of a Human Plasma Ultrafiltrate Bioactive Fraction

Glucocorticoids rapidly inhibit oxytocin-stimulated adrenocorticotropin release from rat anterior pituitary cells, without modifying intracellular calcium transients

Adrenocorticotropin Hyperresponsiveness in Myotonic Dystrophy Following Oral Fenfluramine Administration

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