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PubMed1985

[Hypertrophy of the adrenal cortex].

The human adrenal cortex in essential hypertension and in the salt-losing form of the adrenogenital syndrome and the adrenal cortex in spontaneously hypertensive rats were studied by morphometry. Under long-term functional loading hypertrophy of adrenocortical cells is the common way of increasing the mass of the cortex. The correlation between the morphological parameters of the adrenocortical structures increases in this condition. Hyperplasia along with hypertrophy has been found in man at an early age. The differences in the degree of hypertrophy of the nuclei and nucleoli may be connected with different intensity of adrenocortical function in different pathological conditions.

Adrenal Cortex↗
PubMed2004

An Intrinsic gamma-aminobutyric acid (GABA)ergic system in the adrenal cortex: findings from human and rat adrenal glands and the NCI-H295R cell line.

gamma-Aminobutyric acid (GABA), a major neurotransmitter in the central nervous system, also acts as a paracrine or autocrine signaling molecule in endocrine tissues such as the pancreatic islets, adenohypophysis, and testis. In the present study, we describe local GABA production and functional GABA(B) receptors in the adrenal cortex, possibly forming an auto- or paracrine GABAergic system. Using immunohistochemistry and RT-PCR, we localized the GABA-synthesizing enzyme glutamate decarboxylase 67 and the vesicular GABA transporter in steroid-producing cells of the human and rat adrenal cortex. Immunocytochemistry, Western blots, and RT-PCR experiments demonstrated the presence of glutamate decarboxylase 67 in the human adrenocortical cell line NCI-H295R. Measurements of glutamate decarboxylase activity confirmed that, in these cells and in rat adrenals, glutamate is decarboxylated to form GABA. In addition, we found expression of the GABA(B(1a)), GABA(B(1e)), and GABA(B(2)) subunits of the heterodimeric GABA(B) receptor in NCI-H295R cells as shown by RT-PCR. GABA(B(1a)) and its truncated splice variant GABA(B(1e)) were also found in human and rat adrenal glands. Immunostaining for the GABA(B(2)) subunit revealed its presence in the human and rat adrenal cortex and in NCI-H295R cells. The GABA(B) receptors we identified were functional because the GABA(B) agonist baclofen inhibited T-type Ca(2+) currents in whole-cell patch clamp experiments on NCI-H295R cells. This effect was blocked by pertussis toxin. Furthermore, the alpha(2)-, alpha(3)-, beta(2)-, beta(3)- gamma(2)-, and epsilon-subunits of the GABA(A) receptor were detected in this cell line by RT-PCR. Hence, we conclude that GABA is synthesized and stored by steroid-producing cells of the adrenal cortex and may influence these cells in a paracrine or autocrine manner.

Adrenal Cortex↗
PubMed1981

Immunologic cross-reactivity of the low density lipoprotein receptor from bovine adrenal cortex, human fibroblasts, canine liver and adrenal gland, and rat liver.

An antibody to the low density lipoprotein (LDL) receptor was prepared by immunization of rabbits with a partially purified receptor preparation from bovine adrenal cortex. Immunoglobulin G (IgG) isolated from the serum of immunized rabbits blocked the binding of 125I-LDL to intact bovine adrenal membranes as well as to the partially purified bovine adrenal LDL receptor. The anti-receptor IgG also blocked the binding, uptake, and degradation of 125I-LDL by monolayers of human fibroblasts and thus prevented the LDL-mediated suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase. A monovalent Fab fragment of th anti-receptor IgG retained the ability to inhibit LDL receptors of partially purified bovine adrenal cortex and monolayers of human fibroblasts. By immunofluorescence staining, the anti-receptor IgG was shown to bind to normal fibroblasts in discrete foci that were linearly arranged on the cell surface. No such foci were seen on fibroblasts from a patient with the receptor-negative form of homozygous familial hypercholesterolemia. The rabbit anti-receptor IgG also blocked the binding of 125I-LDL to membranes from dog and rat liver, but it did not prevent LDL binding to rabbit adrenal membranes or rabbit fibroblasts. The immunologic cross-reactivity of LDL receptors from bovine adrenal cortex, human fibroblasts, canine liver and adrenal gland, and rat liver indicates that the structure of this receptor has been widely conserved among animal species and tissues.

Adrenal Cortex↗
PubMedDate not supplied

[The involvement of the cerebral cortex, hypothalamus, pituitary and adrenal cortex in the development of periodontosis].

The authors emphasized in parodontosis patients functional alterations of hypothalamic centres with phagocytosis-stimulatory, vasomotor and neurotrophic functions and disturbances of the functional relationship between the hypothalamus (H), the ascendent reticular formation (RF) and the cerebral cortex (CC). Stimulatory therapy of this areas, especially by direct stimulation of the H improves the hypothalamic functions, the relationship between H and the RF and all the clinical status of parodontosis patients. In rabbits with experimental parodontosis have been found functional and histological alterations in cerebral cortex, and especially in hypothalamus, together with lesions in the hypothalamo-posthypophyso-neurosecretoric system, in the anterior pituitary (P) cells (for ACTH, TSH and FSH) as well as in zona fasciculares of the adrenal cortex (AC). This data, together with findings of other authors, prove that parodontosis is a diencephalopathy involving a whole system: CC-H-P-AC.

Aggressive Periodontitis↗
PubMedDate not supplied

Cytokine expression in the rat adrenal cortex.

The rat adrenal cortex produces the cytokines interleukin-6, tumor necrosis factor, interleukin-1beta, interleukin-1alpha, macrophage migration inhibitory factor, interferon-gamma inducing factor, and transforming growth factor-beta1. Interleukin-6, tumor necrosis factor, and macrophage migration inhibitory factor are localized to the zona glomerulosa. In contrast, interferon-gamma inducing factor is localized to the zona reticularis and fasciculata. Transforming growth factor-beta1 is localized to the zona fasciculata. Endotoxin and interleukin-1 increase interleukin-6 and tumor necrosis factor release from adrenal cells. In contrast, adrenocorticotrophic hormone, adenosine, serotonin, and dopamine increase adrenal interleukin-6 release, but inhibit tumor necrosis factor release. These secretagogues also increase interleukin-6 mRNA content of adrenal cells. Adrenocorticotrophic hormone decreases transforming growth factor beta1 content of adrenal glands. Endotoxin increases adrenal expression of mRNA for macrophage migration inhibitory factor, but decreases the tissue content of this protein. Endotoxin increases the expression of interleukin-1beta mRNA. Cold stress increases the expression of mRNA for interferon-gamma inducing factor. Therefore, cytokines are differentially expressed in the adrenal cortex and the release and production of these cytokines are regulated selectively. Because cytokines have effects on adrenal function and are differentially regulated, they may play autocrine/paracrine roles in regulating the adrenal gland.

Adrenal Cortex↗
PubMed2004

Dependence of fetal hairs and sebaceous glands on fetal adrenal cortex and possible control from adrenal medulla.

Human fetal adrenal development is characterized by rapid growth, high steroidogenic activity, and a distinct morphology, including a unique cortical compartment known as the fetal zone. For most of gestation, the predominant fetal zone accounts for 80-90% of the cortical volume and is the primary site of growth and steroidogenesis, producing 100-200 mg/day of the androgenic steroid, dehydroepiandrosterone sulfate (DHEA-S). The physiological role of this zone during intrauterine life is not well understood. While the glands appear to be capable of DHEA-S synthesis early in gestation (8-10 weeks), we noticed that this event precedes the differentiation of hairs and sebaceous glands. Hairs begin to develop between 9 and 12 weeks and sebaceous glands between 13 and 15 weeks of gestation. Sebaceous glands form an oily secretion - sebum that mixes with desquamated epidermal cells to form vernix caseosa. Vernix caseosa protects the developing skin from constant exposure to amniotic fluid, and hairs helps to hold the vernix caseosa on the skin. We suggest therefore that the human fetal adrenal cortex produces DHEA-S beginning at around 8-10 weeks of gestation in sufficient quantities to influence the growth of hairs and sebaceous glands. Soon after birth, the fetal zone atrophies, and adrenal androgen production decreases to minimal levels. As a consequence, in concordance with the rapid decrease in adrenal androgen levels and in consistent with our hypothesis, fetal hairs are shed and sebaceous glands shrink to small structures. The mechanism that regulates fetal adrenal androgen production is a key unanswered problem in human adrenal biology. Since there exists a close relationship between epinephrine and DHEA-S levels during adrenarche which shows modulatory interactions between adrenal androgen production and adrenomedullary function, we suggest again that adrenomedullary function might play a role in the control of fetal adrenal androgen secretion.

Adrenal Cortex↗
PubMed1990

Immunopathology of adrenal and renal cortical tumors. Coordinated change in antigen expression is associated with neoplastic conversion in the adrenal cortex.

A series of adrenal cortical adenomas (ACA) and carcinomas (ACC), as well as normal adrenal cortex have been studied by a panel of 11 antibodies to characterize antigenic changes that may distinguish these morphologically similar entities. Normal adrenal cortex and ACA express low-molecular weight cytokeratin intermediate filaments. However, none of the six primary or seven metastatic ACCs were found to express detectable levels of cytokeratins. In contrast, vimentin was seen in all ACCs studied and was heterogeneously expressed by ACAs. However, its expression was usually confined to stromal elements of the normal adrenal cortex. We conclude that adrenal cortical cells undergo characteristic changes in intermediate filament expression during the process of neoplastic conversion and malignant transformation. Undetectable expression of cytokeratins and strong expression of vimentin is associated with malignant adrenal cortical lesions. In addition, we examined the antigenic phenotype of a series of primary renal cell carcinomas (RCC). Renal cell carcinomas express cytokeratins, while ACCs do not. The majority of primary RCCs express Lewis blood group isoantigens (most commonly Lewis X), while ACAs and ACCs do not. The panel of antibodies described here may help to distinguish morphologically similar lesions of like histogenesis (ACAs vs. ACCs) and lesions of different histogenesis (adrenal vs. renal) on the basis of their composite antigenic phenotypes.

Adenoma↗
PubMed2005

Adrenal cortex autoantibodies in subjects with normal adrenal function.

The recent advances in our understanding of immunology have greatly improved our knowledge about the natural history of autoimmune diseases and, in particular, of autoimmune Addison's disease (Autoimmune AD). Autoimmune AD is a chronic disorder with a long preclinical period marked by the presence of adrenal cortex autoantibodies (ACAs). In this chapter the main data on this will be analyzed. The populations with the highest risk of Autoimmune AD are first relatives of patients with AAD and patients with autoimmune diseases, particularly those with chronic hypoparathyroidism or with premature ovarian failure. The best markers to identify the subjects at risk are ACAs detected by the immunofluorescence test on human or animal tissues, or 21-hydroxylase autoantibodies (21-OHAbs) detected by radioimmunoassay (RIA). The evaluation of adrenal cortex function in these individuals includes the basal determination of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, plasma renin activity and cortisol after intravenous stimulation with synthetic ACTH. The multivariate analysis of the main factors (genetics, age, gender, titers of antibodies, pre-existing disease, status of the adrenal function) revealed that the risk of future AAD depends only on the presence of high antibody titers, chronic hypoparathyroidism or chronic candidiasis and adrenal dysfunction. On the basis of these parameters the risk of future Autoimmune AD can be calculated with an equation model. Patients with different risk scores need to be monitored at different time intervals, and those at high risk need to be strictly monitored and are the ideal subjects for future prevention trials.

Addison Disease↗