Androstenedione-mediated inhibition of 11β-hydroxylation in monolayer cell cultures of fetal calf adrenals

Baird, Andrew; Kan, Kenneth W.; Solomon, Samuel

doi:10.1016/0022-4731(83)90134-6

Cited by 17 publications

(8 citation statements)

References 15 publications

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“…However, the effect of glucocorticoids could be expressed through direct actions on the adenylate cyclase system and on post-cAMP steps (Darbeida and Durand 1987) or, alternatively, mediated through an enhancement of the responsiveness of adrenal cells to other hormones or factors (present in the culture medium) controlling these steps. Other groups have reported an inhibitory effect of rather high concentrations of glucocorticoids on ACTH-induced adrenal steroidogenesis (Baird et al 1983;Carsia and Malamed 1983;Tim et al 1999). It is shown that only when concentration of Immunoreactive bands for MC2R protein were detected with Western blotting in pig adrenocortical cells.…”

Section: Discussionmentioning

confidence: 94%

“…For example, glucocorticoid receptor (GR) binding sites have been mapped in the adrenal cortex (Loose et al 1980), yet the effects of glucocorticoids in the adrenal cortex are poorly understood. Previous studies suggest that adrenal steroid synthesis is, in part, modulated by steroids synthesized within the adrenal cortex as intermediates or end products (Baird et al 1983;Carsia and Malamed 1983;Tim et al 1999). Most of these studies showed that acute and/or chronic exposure of adrenal cells to exogenous glucocorticoids reduces ACTH-induced steroidogenesis (Carsia and Malamed 1983;Tim et al 1999).…”

Section: Introductionmentioning

confidence: 96%

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Effect of glucocorticoids pretreatment on steroidogenic capacity of adrenocortical cells isolated from Meishan piglets

Yang

et al. 2011

In Vitro Cell.Dev.Biol.-Animal

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The present in vitro experiment was designed to test whether 48 h of pretreatment with glucocorticoids, cortisol, or dexamethasone (DEX), would affect basal and corticotrophin (ACTH) stimulated (24 h) cortisol secretion from primary cultures of pig adrenocortical cells. Cells were divided into six groups: control pretreatment with or without ACTH challenge, cortisol pretreatment with or without ACTH challenge, and DEX pretreatment with or without ACTH. The culture medium and cells were collected at the end of treatment. Cortisol concentration in medium was measured by radioimmunoassay, and protein content of glucocorticoid receptor (GR) and key regulatory factors for steroidogenesis, including melanocortin type 2 receptor (MC2R), steroidogenic acute regulatory protein (StAR) and cholesterol side-chain cleavage cytochrome P450 (P450scc), were detected by Western blot analysis. The results showed that glucocorticoid pretreatment did not affect cortisol secretion under basal condition without ACTH challenge, but significantly enhanced ACTH-stimulated cortisol secretion. Furthermore, the protein content of GR, MC2R, StAR, and P450scc was all increased in groups pretreated with glucocorticoids. These results indicate that adrenocortical cells pretreated with glucocorticoids display higher steroidogenic capacity under ACTH challenge, through the upregulation of GR and other steroidogenic regulatory factors.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 96%

Effect of glucocorticoids pretreatment on steroidogenic capacity of adrenocortical cells isolated from Meishan piglets

Yang

et al. 2011

In Vitro Cell.Dev.Biol.-Animal

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“…However, contrasting evidence was reported. Some investigators reported an inhibition of glucocorticoid secretion when exposed to exogenous corticosteroids (Hill & Singer 1968; Baird et al 1983; Carsia & Malamed 1983), while others reported a stimulation of glucocorticoid secretion with activation of the glucocorticoid receptor (GR) (Darbeida & Durand 1987; Li et al 2011; Asser et al 2014). This discrepancy could be related to the different experimental models used as well as to the concentration and duration of the treatment.…”

Section: Introductionmentioning

confidence: 99%

Regulation of aldosterone secretion by mineralocorticoid receptor–mediated signaling

Chong

Hamid

Yao

et al. 2017

Journal of Endocrinology

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We posit the existence of a paracrine/autocrine negative feedback loop, mediated by the mineralocorticoid receptor (MR), regulating aldosterone secretion. To assess this hypothesis we asked whether altering MR activity in zona glomerulosa (ZG) cells affects aldosterone production. To this end, we studied ex vivo ZG cells isolated from male Wistar rats fed chow containing either high (1.6% Na+ [HS]) or low (0.03% Na+ [LS]) amount of sodium. Western blot analyses demonstrated that MR was present in both the ZG and zona fasciculata/zona reticularis (ZF/ZR/ZR). In ZG cells isolated from rats on LS chow, MR activation by fludrocortisone produced a 20% and 60% reduction in aldosterone secretion basally and in response to angiotensin II (ANGII) stimulation, respectively. Corticosterone secretion was increased in these cells suggesting that aldosterone synthase activity was being reduced by fludrocortisone. In contrast, canrenoic acid, an MR antagonist, enhanced aldosterone production by up to 30% both basally and in response to ANGII. Similar responses were observed in ZG cells from rats fed HS. Modulating glucocorticoid receptor (GR) activity did not alter aldosterone production by ZG cells; however, altering GR activity did modify corticosterone production from ZF/ZR/ZR cells both basally and in response to adrenocorticotropic hormone (ACTH). Additionally, activating the MR in ZF/ZR/ZR cells strikingly reduced corticosterone secretion. In summary, these data support the hypothesis that negative ultra-short feedback loops regulate adrenal steroidogenesis. In the ZG, aldosterone secretion is regulated by the MR, but not the GR, an effect that appears to be secondary to a change in aldosterone synthase activity.

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“…Thus from these experiments it appears most likely that llß,17ß,dihydrQxy-4-androsten-3-pne is mainly a secretory product of the adrenal gland, and that this steroid is a specific marker of adrenal functiori. Furthermore, 11 ß,l 7ß-dihydroxy-4-androsten-3-one might be of interest in regard to the autoregulation of steroidögenesis in the adrenal gland by modifyirig enzyme activities (11,12).…”

Section: Discussionmentioning

confidence: 99%

The Measurement of 11ß, 17ß-Dihydroxy-4-androsten-3-one (11ß-Hydroxytestosterone) by Radioimmunoassay in Human Plasma

Schlaghecke¹,

Kley²,

Krüskemper³

1986

Clinical Chemistry and Laboratory Medicine

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Summary: A radioimmunoassay (RIA) is described for the measurement of llß,17ß-dihydroxy-4-androsten-3-one (llß-hydroxytestosterone) in human plasma. The reliability criteria of the new RIA were similar to those of other steroid hormone radioimmunoassays. The mean plasma llß,17ß-dihydroxy-4-androsten-3-one level for healthy young subjects was 1.31 ± 0.32 nmol/1 (x ± SD) in males and 1.19 ± 0.35 nmol/1 in females at 8 a. m.; during the night, there was a marked decrease, and at 11 p. m. the recorded values were 0.41 ± 0.15 nmol/1 and 0.46 ± 0.14 nmol/1, respectively. During the corticotropin Stimulation test, llß,17ß-dihydroxy-4-androsten-3-one increased from 1.03 ± 0.33 nmol/1 to 1.31 ± 0.41 nmol/1, while in dexamethasone suppression tests a decrease from 2.04 ± 0.82 nmol/1 to 0.25 ± 0.05 nmol/1 was seen. In contrast, | chorionic gonadotropin administration on 3 consecutive days did not influence plasma concentrations of f 11 ß,17ß-dihydroxy-4-androsten-3-one. Radioimmunoassay zur Messung von llß f i7ß-Dihydroxy-4-androsten-3-on (llß-Hydroxytestosteron) im Plasma des MenschenZusammenfassung: Es wird ein Radioimmunoassay für die Messung von llß,17ß-Dihydroxy-4-androsten-3-on (llß-Hydroxytestosteron) im menschlichen Plasma beschrieben. Die Zuverlässigkeitskriterien des neu aufgebauten RIA entsprechen denen anderer Radioimmunoassays für Steroidhormone.Die Konzentration von llß,17ß-Dihydroxy-4-androsten-3-on betrug um 8.00 Uhr im Plasma gesunder Männer 1,31 + 0,32 nmol/1 ( ± SD) und bei gesunden Frauen 1,19 ± 0,35 nmol/1. Um 23.00 Uhr fanden ; sich 0,41 ± 0,15 nmol/1 (Männer) und 0,46 ± 0,14 nmol/1 (Frauen). Im Cörticotropin-Stimulationstest war ein Anstieg der Konzentration von llß,17ß-Dihydroxy-4-androsten-3-on im Plasma von 1,03 ± 0,33 nmol/1 | auf 1,31 ± 0,41 nmol/1 zu beobachten, während sich im Dexamethasontest ein Rückgang von 2,04 ± 0,82 ! nmol/1 auf 0,25 ± 0,05 nmol/1 ergab. Nach Applikation von Choriongonadotropin wurde keine Änderung i der Konzentration von llß,17ß-Dihydroxy-4-androsten-3-on gemessen. IntroductionRecently 17ß-hydroxy-4-androstene-3,ll-dione and The adrenal atidrogens are quantitatively the most 4-androstene-3, 11,17-trione were demonstrated in important steroid hormones but their physiological human plasma (2, 3). In contrast, no Information role reniains still somewhat obscure in man. Far less is ayailable about llß,17ß-dihydroxy-4-androsten-3-information is available about the adrenal androgens one in human peripheral blood. The present paper that carry a functional group at C-ll. llß-Hydroxy-describes a radioimmunoassay system for the meas-4-androstene-3,17-dione has been demonstrated in urement of llß,17ß-dihydroxy-4-androsten-3-one, human plasma and might play an important role and presents the fürst published values for this androunder physiological and pathological conditions (1). gen in human plasma.

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Androstenedione-mediated inhibition of 11β-hydroxylation in monolayer cell cultures of fetal calf adrenals

Cited by 17 publications

References 15 publications

Effect of glucocorticoids pretreatment on steroidogenic capacity of adrenocortical cells isolated from Meishan piglets

Effect of glucocorticoids pretreatment on steroidogenic capacity of adrenocortical cells isolated from Meishan piglets

Regulation of aldosterone secretion by mineralocorticoid receptor–mediated signaling

The Measurement of 11ß, 17ß-Dihydroxy-4-androsten-3-one (11ß-Hydroxytestosterone) by Radioimmunoassay in Human Plasma

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