Dexamethasone suppression of adrenocortical function.

A M Sharp; D J Handelsman; R M Ristuccia; J R Turtle

Home/Archive/PubMed

PubMed · 6280896

Dexamethasone suppression of adrenocortical function.

A M Sharp·D J Handelsman·R M Ristuccia·J R Turtle

View original source ↗Export metadata ↓

Abstract

To investigate the potency of dexamethasone in suppressing adrenocortical function, we gave various evening doses to laboratory staff members. Plasma corticotropin, cortisol, and dehydroepiandrosterone sulfate concentrations were measured the following day, to quantitate the degree of suppression after both short- and long-term treatments. We found that the minimum amount for effective suppression was 1 mg for a single evening dose, 0.5 mg per day for a long-term evening dose. On these regimens plasma corticotropin and cortisol were consistently suppressed, but plasma dehydroepiandrosterone sulfate was suppressed only with long-term treatment.

Explore related subjects

Adrenal Cortex Adrenal Cortex Function Tests Adrenocorticotropic Hormone Adult Dehydroepiandrosterone Depression, Chemical Dexamethasone Humans Hydrocortisone Time Factors Comparative Study Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

A M Sharp, D J Handelsman, R M Ristuccia, J R Turtle. 1982. Dexamethasone suppression of adrenocortical function.. https://pubmed.ncbi.nlm.nih.gov/6280896/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Immunohistochemical Jun/Fos protein localization and DNA synthesis in rat adrenal cortex after treatment with ACTH or FGF2.

In vitro and in vivo studies have suggested that the expression of the early response genes for Jun and Fos proteins plays an important role in adrenal cell proliferation. In order to study the expression pattern of the activating protein-1 (AP-1) family of oncogenes in the adrenal gland, we have used immunohistochemistry to localize Jun and Fos protein expression in rat adrenal cortex infused in situ with adrenocorticotropic hormone (ACTH), fibroblast growth factor 2 (FGF2), or both. The expression of AP-1 factors has been found to be correlated with in vivo ACTH and FGF2 proliferation in rats treated with dexamethasone and bromodeoxyuridine (BrdU). Induction of c-Jun and c-Fos in the zona fasciculata and of FosB in the zona reticularis suggests that, after ACTH stimulation, these proteins are the main AP-1 components in these zones. In vivo, ACTH increases BrdU-positive cells in the zona fasciculata and zona reticularis suggesting that the composition of AP-1 complexes in these zones is correlated with proliferation. Patterns of Fos and Jun induction by FGF2 do not resemble those after ACTH induction. However, in isolation, neither affects the zona glomerulosa. In the zona fasciculata, and more so in the zona reticularis, FGF2 modulates responses to ACTH, reducing the numbers of Jun-positive cells, Fos-positive cells, and DNA synthesis. This indicates that FGF2 antagonizes ACTH, and that ACTH thus controls the trophic effect independently of exogenous FGF2. Our results implicate the AP-1 family of transcription factors in the regulation of cell progression and the control of ACTH-induced proliferation in the zona fasciculata and zona reticularis.

Adrenal Cortex↗

PubMed2007

Tyrosine phosphatases in steroidogenic cells: regulation and function.

In adrenocortical and Leydig cells PKA activation by trophic hormones increases the activity of protein tyrosine phosphatases and also induces the expression of MAP kinase phosphatase 1 (MKP-1), a dual activity protein phosphatase (serine/threonine and tyrosine). This work summarizes the knowledge on the regulation and the role played by cAMP-activated tyrosine phosphatases as well as MKP-1 in the hormonal activation of the acute and chronic phases of steroidogenesis.

Adrenal Cortex↗

PubMed2007

Stimulation of the pituitary-adrenal axis and of adrenocortical steroidogenesis ex vivo by administration of di-2-ethylhexyl phthalate to prepubertal male rats.

Phthalate esters exert deleterious effects on testicular physiology and, consequently, on reproduction and fertility. However, little is presently known concerning potential adverse effects of these environmental pollutants on the hormonal functions of the adrenal gland. Therefore, we have investigated the effects of administering to rats of different developmental ages di-2-ethylhexyl phthalate (DEHP) on the hypothalamic-pituitary-adrenal axis in vivo, as well as on adrenocortical steroidogenesis ex vivo. Oral exposure to DEHP once daily for 4 days elevated the serum levels of ACTH and corticosterone in rats 20 and 40 days of age, but not in adult, 60-day-old animals. Furthermore, primary cultures of adrenocortical cells isolated from 20- and 40-day-old rats treated with DEHP exhibited an enhanced capacity to produce corticosterone in response to ACTH, dibutyryl cAMP, and 22R-hydroxycholesterol, as well as increased ACTH-stimulated transport of endogenous cholesterol into mitochondria. Neither DEHP nor its major metabolite mono-2-ethylhexyl phthalate altered steroidogenesis in cultures of adrenocortical cells isolated from untreated rats. These findings demonstrate that in male rats, DEHP exerts an age-dependent influence on the pituitary-adrenocortical axis in vivo and adrenocortical steroidogenesis ex vivo. Such perturbation may be of pathological significance in connection with disorders of the hormonal stress response, especially in very young human beings.

Adrenal Cortex↗