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PubMed1991

Different roles for the pituitary and adrenal cortex in the control of enkephalin peptide localization and cortico-medullary interaction in the sheep adrenal during development.

We have investigated the effect of adrenocorticotrophic hormone (ACTH) replacement after fetal hypophysectomy on the pattern of localization of enkephalin-containing peptides (enkephalins) and phenylethanolamine N-methyltransferase (PNMT) in the fetal sheep adrenal. We have also investigated the relative roles of the fetal pituitary and adrenal cortex in determining the extent of the interdigitation of the peripheral adrenaline (AD)-containing cells of the adrenal medulla with the inner zones of the adrenal cortex in the late gestation fetus. Fetal hypophysectomy (Hx; n = 12) or sham operations (n = 8) were performed at 109-118d. At 138 or 139d, ACTH (1-24) (10.5 micrograms/h) was infused intravenously for 72 h into 4 Hx fetuses (Hx + ACTH group). Saline was infused for 72 h into 4 Hx fetuses (Hx + Sal) and into 4 sham-operated fetal sheep (Intact + Sal). Fetal adrenal glands were collected at autopsy from 141/2d Intact + Sal, Hx + Sal and Hx + ACTH groups, from 4 intact fetal sheep at 145-147d gestation (145/7d Intact group) and 4 Hx fetal sheep at 147-164d gestation (147/64d Hx group). Adrenals were also collected from 4 newborn lambs at 10-12d after birth (10/12d Newborn group). Using the peroxidase-antiperoxidase immunocytochemical staining method, sections of adrenal glands (10-12 microns) from all groups were stained anti-PNMT. Sections of adrenal glands from the 141/2d groups were also stained separately with anti-dopamine-beta-hydroxylase (anti-D beta H) and anti-enkephalin (anti-ENK).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1981

Development of the adrenal cortex in the fetal foal: an ultrastructural study.

The adrenal cortex from twelve fetal foals (gestational ages from 61 to 300 days) was examined by light and electron microscopy. Adrenal glands from three newborn foals were also examined by light microscopy. Between 61 and 100 days of gestation the adrenal cortex became organised into two distinct regions, the zona glomerulosa and zona fasciculata, which grew steadily in thickness until the 300th day. Between 300 days and birth there was a dramatic increase in the width of the zona fasciculata. From 200 days a narrow band of compact cells marked the cortico-medullary border. Though these cells were ultrastructurally indistinguishable from those of the overlying zona fasciculata it seems possible that they may later give rise to the zona reticularis of the adult gland. The cells of the zona glomerulosa were columnar in shape and were tightly packed together into cell clusters. They contained smooth and rough endoplasmic reticulum and mitochondria with lamellar cristae. The ultrastructural characteristics of the cells of the zona glomerulosa changed little throughout the course of gestation. In the zona fasciculata the predominant cell type was angular in profile, and its cytoplasm contained smooth and rough endoplasmic reticulum and mitochondria with lamellar cristae. The second and larger cell type was situated nearer the cortico-medullary border. It contained an abundance of smooth endoplasmic reticulum, mitochondria with lamellar and/or vesicular cristae, and large perinuclear Golgi complexes. These cells, which appeared to be derived from the smaller more angular cells of the zona fasciculata, showed signs of a high level of metabolic and synthetic activity. As gestation progressed the number of functionally differentiated cells increased slowly in a radial direction towards the zona glomerulosa. Indirect evidence from two newborn foals suggests a rapid increase in the functional differentiation of zona fasciculata cells between 300 days and birth.

Adrenal Cortex↗
PubMed2001

The role of the adrenal cortex in polycystic ovary syndrome.

Adrenal androgen excess affects approximately 25% of PCOS patients. The exact etiology of this excess in PCOS patients is unclear. Some evidence that adrenal androgen excess may be a genetic trait. The adrenal androgen response to ACTH is highly individualized, and the relative response seems to be constant over time. In addition, there is a strong familial component to adrenal androgen levels in normal individuals and PCOS patients. It is possible that the tendency to overproduce adrenal androgens is an inherited risk factor for the development of PCOS. Overall, few hyperandrogenic patients actually have isolated deficiencies of 3 beta-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11-hydroxylase. The ovarian hormonal secretion in PCOS can affect adrenal androgen secretion and metabolism, although this factor accounts for only part of this abnormality. More likely, the adrenal androgen excess results from a generalized hyperresponsiveness of the adrenal cortex to ACTH, but without an increase in CRH or ACTH sensitivity. Although glucocorticoid administration may improve the ovulatory function of these patients, the results are modest and cannot be predicted by the circulating androgen levels.

Adrenal Cortex Diseases↗
PubMed1980

[Adrenal cortex function in trophoblastic disease].

In 100 patients with trophoblastic tumors the functional activity of the adrenal cortex was examined before and after chemotherapy. Androgen-producing function of the adrenal cortex was found to be reduced as well as the absolute number of excreted 17-ketosteroids separate fractions and their ratio. The glucocorticoid function of the adrenal cortex shows a monotonous character. Only in patients having uterine chorion-epithelioma with metastases a reliable reduction of the fraction of 11-hydroxy-17-ketosteroids is noted before and after chemotherapy, while the per cent content of free 17-oxy-corticoid fraction is increased with regard to their total amount. Successful chemotherapy, associated with a lower titre of chorionic gonadotropins up to its complete disappearance, does not result in normalization of values characterizing the functional activity of the adrenal cortex.

17-Hydroxycorticosteroids↗
PubMed2000

Different pathways of neurohormonal hypothalamic control of the adrenal cortex function in young and old rats.

The pathways of hypothalamic control of the adrenal cortex function were studied in the experiments on young and old male Wistar rats. Immunohistochemical, morphometric, densitometric and radioimmunoassay methods were used. It was shown that in young rats under stress vasopressin (VP) is released into the portal circulation and probably in this way stimulates ACTH and enhances secretion of corticosterone in the adrenal cortex. In old rats stress-reaction is delayed and less adequate compared to young animals. It seems likely that in old rats VP is secreted into the general circulation mainly via the posterior pituitary lobe (PP), exerting a direct influence on the adrenal cortex. The conclusion is made that in old rats regulation of the adrenal cortex function is realised via the pathway phylogenetically more ancient than in young animals.

Adrenal Cortex↗
PubMed1985

Identification of D-2 dopaminergic receptors in bovine adrenal cortex.

Dopamine receptors in bovine adrenal cortex have been studied by using 3H-(-)sulpiride as selective ligand. The specific binding is saturable and the Scatchard analysis reveals a single component with a Kd of 6.2 nM and a Bmax of 8 fmoles/mg protein. The characterization indicates that the binding is rapid, reversible, stereospecific, Na+ - and temperature- dependent. Moreover its pharmacological profile is superimposable to that of D-2 receptors in the striatum, thus suggesting that central and peripheral D-2 receptors are identical.

Adrenal Cortex↗
PubMed1984

Transaminative pathway of glutamate oxidation in adrenal-cortex mitochondria.

Mitochondria isolated from adrenal cortex of beef do oxidize glutamate if the amino group acceptor-oxaloacetate (or its precursor-malate) is present in the incubation medium. The glutamate (plus oxaloacetate) oxidation was enhanced by ADP or deoxycorticosterone, indicating that this respiration can support both oxidative phosphorylation and 11 beta-hydroxylation of deoxycorticosterone to corticosterone. Avenaciolide (inhibitor of glutamate entry into the mitochondria), aminooxyacetate (inhibitor of aspartate aminotransferase activity) and arsenite (inhibitor of 2-oxoglutarate dehydrogenase) when introduced into the incubation media before respirating substrates, inhibited the ability of ADP or deoxycorticosterone to stimulate the rate of glutamate (plus oxaloacetate) oxidation.

Adrenal Cortex↗
PubMed1982

Pregnenolone efflux from mitochondria of bovine adrenal cortex.

Pregnenolone efflux from bovine adrenal cortex mitochondria was measured with the aid of rapid separation of the organelles from the incubation by centrifugation through silicon oil. In the absence of bovine serum albumin or cytosolic supernatant (100 000 x g), an equilibrium distribution of newly synthesised pregnenolone was attained after 2 min at 30 degrees C; 20% of total pregnenolone was located outside the mitochondria. The presence of 13 mg albumin/ml or 13 mg supernatant protein/ml increased the exogenous proportion of pregnenolone to over 90% and 75% respectively without affecting the rate of cholesterol side-chain cleavage. The binding of pregnenolone by both albumin and supernatant was non-specific and non-saturable. It is suggested that in vivo the mitochondrial membranes do not present a significant barrier to pregnenolone efflux from the organelle.

Adrenal Cortex↗
PubMed1984

[Pyruvate kinase in the bovine adrenal cortex].

Pyruvate kinase from bovine adrenal cortex was purified to an electrophoretically homogeneous state. The molecular weight of the native enzyme is about 230 000, that of one subunit is 57 000. The maximal values of the pyruvate kinase initial reaction rate were obtained in 50 mM imidazole-acetate buffer within the pH range of 6.8 to 7.0. The curve of the initial pyruvate kinase reaction rate versus phosphoenolpyruvate (PEP) and ADP concentrations is hyperbolic and obeys the Michaelis-Menten kinetics with Km for PEP and ADP of 0.055 X 10(-3) M and 0.25 X 10(-3) M, respectively. The enzyme is activated by Mn2+ and Co2+ by 43 and 38%, respectively. IDP, GDP, and UDP may be used as analogs of ADP. The enzyme is not activated by fructose-1.6-diphosphate and is inhibited by L-phenylalanine and ATP.

Adenosine Triphosphate↗
PubMed1988

[Ultrastructural characteristics of the microcirculatory bed of the human adrenal cortex in prenatal ontogenesis].

By means of transmissive electron microscopy the adrenals have been studied in 25 human embryos and fetuses at the age of 6-36 weeks. Certain stages have been revealed in formation of the adrenal cortex microcirculatory bed. In 6-7-week-old embryos (period of diffuse protocapillary bed) endothelial structure and mesenchymal cells, surrounding the adrenal anlage, resemble one another. A distinguished feature of the endothelium is regularly revealed desmosomes and large vacuoles, often found in cytoplasm of endotheliocytes. In 8-12-week-old fetuses (period when the organospecific microcirculatory bed is forming) sinusoid capillaries differentiate in the internal zone of the adrenal cortex; in endothelium fenestrae, "hatches", "locks" are revealed, the capillary basal membrane is formed. During subsequent time of the intrauterine development perfection of the microcirculatory pathways in the adrenals takes place, the arteriolar link of the subcapsular layer including. By the time of birth morphofunctional maturity of the microcirculatory bed in the adrenal cortex is noted.

Adrenal Cortex↗
PubMed1981

The effect of azastene, cyanoketone and trilostane upon respiration and cleavage of the cholesterol side chain in mitochondria from bovine adrenal cortex.

Mitochondria prepared from bovine adrenal cortex and incubated with ADP and phosphate respired at about 45% of the rat observed in the presence of an uncoupler of oxidative phosphorylation; there was, however, little inefficiency in the reactions involved in the phosphorylation of ADP. Three inhibitors of the 3 beta-hydroxysteroid dehydrogenase (azastene, cyanoketone and trilostane) were employed with a view to preventing pregnenolone metabolism and thus aiding the assay of cholesterol side-chain cleavage. Freshly made solutions of these inhibitors did not modify mitochondrial respiratory rates, at concentrations of 10 microM. In contrast, solutions maintained at 0-4 degrees C for one week subsequently inhibited the respiratory rate of uncoupled mitochondria. When fresh solutions of the inhibitors were used in the assays of cholesterol side-chain cleavage, 10 microM azastene did not significantly inhibit pregnenolone metabolism. Cyanoketone and trilostane were both significant inhibitors of pregnenolone metabolism, but 10 microM cyanoketone reduced the initial rate of cholesterol side-chain cleavage by 50% in the presence of 10 mM malate, although this inhibition did not occur in the presence of 10 mM DL-isocitrate. Thus trilostane may be the preferred inhibitor of the 3 beta-hydroxysteroid dehydrogenase during studies of cholesterol side-chain cleavage in vitro.

Adrenal Cortex↗