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At least 811 records · Page 45Linked to original sources
PubMed1994

[The effects of electroacupuncture treatment on nucleolar organizer regions of adrenal cortex in ovariectomized rats].

The present paper reports the morphometric analysis of nucleolar organizer regions (NORs) of the adrenal cortex in ovariectomized rats following electroacupuncture (EA) using argyrephil (Ag-NOR) method for NORs. Animals were divided into four groups, the control group (CT group, n = 4), the EA group (n = 3), the ovariectomized group (OV group, n = 4) and the ovariectomized electroacupuncture group, (OV+EA group, n = 7). The number of AgNORs of 100 cells from zona fasciculata of the adrenal cortex in each case of all groups was counted at random and the mean +/- SE (number/cell) in each group was calculated as follows: OV+EA group 2.71 +/- 0.26, OV group 1.62 +/- 0.15, EA group 1.21 +/- 0.04 and CT group 1.48 +/- 0.03. The mean of AgNORs in OV+EA group differed highly significantly from the other three groups (P < 0.01) tested by ANOVA and LSD method, No significant distinction was found among the OV group, EA group and CT group. Gross specimen examination showed that adrenal glands in OV+EA were significantly heavier than those in the other three groups (P < 0.01). Vaginal smears showed that a response like that of estrogen-induced with exfoliative cells appeared in the OV+EA group rats following EA. EA had no influence on the change of exfoliative cells in EA group. The results suggest that EA may promote the synthesis and secretion of the adrenal steroid hormones, the androgen of which will then be transformed into estrogen in other tissues, thus compensating the deficiency of estrogen induced by ovariectomy.

Adrenal Cortex↗
PubMed2004

Dual hormonal regulation of endocrine tissue mass and vasculature by adrenocorticotropin in the adrenal cortex.

The mass of healthy adult tissues is stable and their vasculature is quiescent, but this equilibrium is disrupted under certain physiological or pathological situations. There is an emerging concept indicating that these trophic changes may be initiated by modifications of the vasculature. In the current study, we documented over a period of 14 d the serial alterations occurring in both endocrine and endothelial compartments during adrenal atrophy induced by ACTH suppression in mice. After dexamethasone perfusion, a rapid fall of plasmatic ACTH and corticosterone concentrations was observed within the first 24 h. During the first 4 d of treatment, adrenal weight and adrenal cortex cellularity decreased rapidly. This was correlated with an inhibition of cell proliferation and a massive induction of endocrine cell apoptosis. Between d 4 and d 14, a slower but sustained decay of adrenal cortex size and cellularity was observed. This second phase was associated with progressive loss of vascular endothelial growth factor protein expression in the endocrine cells and regression of the vascular network. These data support the concept that ACTH controls adrenal cortex trophicity through a dual mechanism involving its antiapoptotic effect on endocrine cells and its indirect vascular endothelial growth factor-mediated action on endothelial cells.

Adrenal Cortex↗
PubMed1979

Solubilization of membrane-bound adenylate cyclase of isolated rat adrenal cortex cells.

The membrane-bound adenylase cyclase (ATP pyrosphosphate-lyase (cyclizing), EC 4.6.1.1) of isolated rat adrenal cortex cells can be rendered soluble using 0.02 M Lubrol 12A9. The solubilized enzyme can be filtered through Milipore filters with pores 0.22 micron in diameter. Using gel filtration, on Sephadex G-200, adenylate cyclase activity was eluted with a distribution coefficient of 0.139, whereas on Sephadex G-100 the activity was eluted in the excluded volume. Half-maximum activation of the postulated guanyl nucleotide regulator site of adenylate was achieved with 5'-guanylyl-imidodiphosphate at a concentration of 1 . 10(-6)M. In contrast, however, using intact isolated rat adrenal cortex cells the guanyl nucleotide regulator site could not be stimulated by 5'-guanylyl-imidodiphosphate.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1987

Adenylate cyclase of bovine adrenal cortex plasma membranes. Divergence between corticotropin and fluoride combined effects with forskolin.

The diterpene forskolin maximally stimulated bovine adrenal cortex adenylate cyclase activity 9-fold with a concentration producing half-maximum effect (ED50) of about 4 microM. The effects of forskolin and the fully active corticotropin fragment ACTH (I 24) were additive over nearly the whole range of concentration of both effectors, indicating separate and independent mechanisms of action. By contrast, 10 mM NaF blocked forskolin action in the nanomolar range of the diterpene concentration, while it allowed a partial stimulation by forskolin in the micromolar range. NaF thus reveals a heterogeneity of forskolin action in the adrenal cortex plasma membranes. Moreover, our data suggest that ACTH and NaF activation effects, both mediated by the stimulatory regulatory protein Gs, proceed through different mechanisms.

Adenylyl Cyclases↗
PubMed1999

Anatomical and functional demonstration of a multisynaptic suprachiasmatic nucleus adrenal (cortex) pathway.

In view of mounting evidence that the suprachiasmatic nucleus (SCN) is directly involved in the setting of sensitivity of the adrenal cortex to ACTH, the present study investigated possible anatomical and functional connections between SCN and adrenal. Transneuronal virus tracing from the adrenal revealed first order labelling in neurons in the intermedio-lateral column of the spinal cord that were shown to receive an input from oxytocin fibres and subsequently second-order labelling in neurons of the autonomic division of the paraventricular nucleus. The latter neurons were shown to receive an input from vasopressin or vasoactive intestinal peptide (VIP) containing SCN efferents. The true character of this SCN input to second-order neurons was also demonstrated by the fact that third-order labelling was present within the SCN, vasopressin or VIP neurons. The functional presence of the SCN-adrenal connection was demonstrated by a light-induced fast decrease in plasma corticosterone that could not be attributed to a decrease in ACTH. Using intact and SCN-lesioned animals, the immediate decrease in plasma corticosterone was only observed in intact animals and only at the beginning of the dark period. This fast decrease of corticosterone was accompanied by constant basal levels of blood adrenaline and noradrenaline, and is proposed to be due to a direct inhibition of the neuronal output to the adrenal cortex by light-mediated activation of SCN neurons. As a consequence, it is proposed that the SCN utilizes neuronal pathways to spread its time of the day message, not only to the pineal, but also to other organs, including the adrenal, utilizing the autonomic nervous system.

Adrenal Cortex↗
PubMed2002

Human adrenal cortex and aldosterone secreting adenomas express both 11beta-hydroxysteroid dehydrogenase type 1 and type 2 genes.

11beta-Hydroxysteroid dehydrogenase type 1 and type 2 (11betaHSD1 and 11betaHSD2) isozymes catalize the conversion of inactive glucocorticoids (e.g. cortisone) to their active forms (e.g. cortisol) and vice versa, respectively. Reverse transcription-polymerase chain reaction allowed the detection of 11betaHSD1 and 11betaHSD2 mRNAs in the human adrenal cortex, liver, kidneys, as well as in six aldosterone-secreting adenomas. 11betaHSD1 and 11betaHSD2 activity, as evaluated by the capacity of the microsomal fraction to convert [3H]cortisone to [3H]cortisol and vice versa, was detected in both human adrenal cortex and aldosteronomas, although it was less elevated than in liver and kidneys. Aldosteronomas possessed more intense 11betaHSD1 activity and less intense 11betaHSD2 activity than the normal adrenal cortex. The hypothesis is advanced that the elevated local concentration of steroid-hormone intermediates occurring in aldosteronomas up-regulates 11betaHSD1 and down-regulates 11betaHSD2, thereby contributing to their enhanced steroidogenic function.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMedDate not supplied

[Features of the structure of the adrenal cortex in domesticated Vulpes fulvus silver foxes during postnatal ontogeny].

Studies have been made on the structure of the adrenal cortex in relatively wild and domesticated male and female silver foxes at the age of 1-7 days, 1, 2 and 8 months. It was demonstrated that during domestication, deep morphological changes in the adrenal cortex take place which indicate the decrease of functional activity in the fascicular zone and the increase of the activity in the reticular zone. Differences found in the first days of postnatal life become more evident in further ontogenesis.

Adrenal Cortex↗
PubMed1988

Stimulatory effect of prolactin on the mitotic activity of the adrenal cortex in snell mice with hereditary dwarfism.

Effects of thyrotropin (TSH), growth hormone (GH), prolactin (Prl), and ACTH on the proliferation of adrenocortical cells in male Snell dwarf mice and in phenotypically normal male mice from the same strain were examined by means of the colchicine metaphase-arrest technique. After 6 days of treatment, ACTH increased significantly the mean mitotic activity rate (MMAR) of adrenocortical cells in both the normal (nondwarf) and dwarf mice as compared to the corresponding control groups receiving physiologic saline. None of the remaining examined pituitary hormones did exert a mitogenic action on the adrenal cortex of normal mice. It was, however, recorded the significant elevation of the MMAR of the adrenocortical cells in Prl-treated Snell dwarf mice, while TSH and GH did not stimulate mitogenesis. The acquired data corroborates a well-known proliferogenic effect of ACTH on the adrenal cortex in vivo. The increase of the MMAR of the adrenal cortex of Snell dwarfs following Prl-treatment is in agreement with earlier reports.

Adrenal Cortex↗
PubMedDate not supplied

[Effect of alpha-tocopherol on adrenal cortex functions under stress].

alpha-Tocopherol has been studied for its effect on lipid peroxidation and steroidogenesis in the adrenal cortices of rat and rabbit under stress. The vitamin is shown to exert an inhibitory effect on the lipid peroxidation developing under chronic stress. A biphasic pattern of the alpha-tocopherol effect on the steroidogenesis in the adrenal cortex is established: a decrease in the release of the steroids under the acute stress and maintaining of their levels under the chronic stress. A conclusion is drawn about a potential alpha-tocopherol application to correct the adrenal cortex function under stress.

Adrenal Cortex↗
PubMed2003

Transcription factor 3',5'-cyclic adenosine 5'-monophosphate-responsive element-binding protein (CREB) is decreased during human adrenal cortex tumorigenesis and fetal development.

Various cellular and molecular alterations of the cAMP pathway have been observed in adrenal Cushing syndrome. We recently reported the loss of cAMP-responsive element-binding protein (CREB) expression in the adrenocortical cancer cell line H295R. CREB is the major nuclear target of the cAMP pathway. This study therefore aimed to analyze the status of the CREB protein in various types of human adrenocortical tumors and normal fetal adrenal cortex. CREB protein status was studied by Western blotting in adrenocortical adenomas (AAs, n = 27) and adrenocortical carcinomas (ACs, n = 24). A decrease of CREB protein was noticed in the majority of the adrenocortical tumors. The dramatic decrease in CREB protein levels was more pronounced in ACs than in AAs. Levels of the phosphorylated form of CREB were also low in adrenocortical tumors, with a greater decrease in ACs than in AAs. EMSAs also showed decreases in the amounts of CREB- containing complexes in nuclear extracts from adrenocortical tumors. The secretory status of adenomas was strongly correlated with CREB levels, significantly lower in nonfunctioning AAs (n = 9) than in functioning AAs (n = 9). CREB levels, determined by Western blotting and immunohistochemistry, were very low in the fetal zone of human fetal adrenal cortex, whereas they were normal in the definitive zone. In tumors, adrenocortical cells in several zones were weakly immunohistochemically stained for CREB, whereas CREB was uniformly detected in nonendocrine cell nuclei (e.g. vascular cells, fibroblasts). These results suggest that the absence of CREB may be linked to the development of a highly aggressive tumor with a dedifferentiated benign (nonfunctioning AA) or malignant (AC) phenotype. These findings highlight the similarities between the normal human fetal adrenal gland and adrenal cancers previously observed in terms of parallelism in IGF-II production.

Adolescent↗