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Results for “ADRENAL CORTEX”

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At least 1,369 records · Page 76Linked to original sources
PubMed1981

[Functional-morphologic features of the adrenal cortex in white rats during protracted exposure to styrene].

Experiments on rats showed that long-term styrene exposure suppresses both specific and nonspecific cell metabolic indices in different adrenocortical areas. However, the sensitivity of the different areas proved to vary under styrene exposure. This allows the suggestion that each area undergoes different degree of damage which brings about the disturbance of optimum correlations between various functions of the adrenal cortex. Administration of metapirone during the first weeks of exposure diminishes the main effect of styrene. It is concluded that one of the possible factors leading to the development of abnormalities under chronic exposure to aromatic hydrocarbons may involve the breach of the correlations between different structural components of the adrenal cortex thereby favouring the maintenance of the whole body discordance.

Acid Phosphatase↗
PubMed1980

Sex differences in adrenocortical structure and function. VI. Long-term effect of gonadectomy and testosterone or estradiol replacement on rat adrenal cortex.

Gonadectomy or sham operations were performed on rats of Wistar strain weighing 150--170 g. Animals were sacrificed in groups, males 397 days and females 395 days after surgery. 14 days before autopsy some of the gonadectomized rats were injected with a single dose of depo-testosterone or depo-estradiol respectively. Absolute as well as relative adrenal weights were larger in female than in male rats. Long-term orchiectomy did not change these weights while testosterone, if compared with control, lowers the weights of the adrenals. Long-term ovariectomy lowers the weights of the glands and estradiol reversed them to the control level. Adrenal cortex of rats studied show irregular zonation. Within the zona fasciculata two types of cells were observed--with strongly eosinophilic and pale cytoplasm. In some cases groups of hypertrophied cells surrounded by spindle-shaped cells were observed. Neither long-term gonadectomy nor gonadal hormone replacement has a marked effect on the structure of the adrenal cortex. In male and female rats there was no difference in the volume of single zona fasciculata and reticularis cells. Long-term orchiectomy has no effect on this volume while testosterone resulted in a lowering of volume of zona fasiculata cells. Neither long-term ovariectomy nor estradiol has an effect on morphometric parameters studied in the fasciculata and reticularis zones. Distinct sex differences and dependence on sex hormones were found in reactions for alpha-glycerophosphate dehydrogenase and nonspecific esterases activity.

Adrenal Cortex↗
PubMedDate not supplied

Relationship between adrenal cortex pathology in Cushing's syndrome and its response to the dexamethasone suppression test.

Cushing's syndrome is a severely disabling condition which can cause death if left untreated. Endogenous Cushing's syndrome can be ACTH-dependent or ACTH-independent. The ACTH-dependent type is more common and is usually caused by diffuse hyperplasia on the adrenal cortex. This study investigated the response to low- and high-dose dexamethasone suppression testing of 30 adrenalectomized patients with Cushing's syndrome, average age 37.3 +/- 9.7 years. Twenty-four (79.3%) patients were female, and six (20.7%) were male. Bilateral adrenalectomy was performed in 14 (48.2%) patients and unilateral adrenalectomy (nine and seven right adrenalectomy) in 16 (51.8%). Two of the bilateral adrenalectomies were applied via endoscopic surgical approach. In the histopathological evaluation, diffuse hyperplasia was diagnosed in 13 (44.8%) patients and nodular hyperplasia in eight (26.6%), three macronodular and five micronodular hyperplasia. Adrenal cell adenoma was diagnosed in nine (28.6%) patients. Classic dexamethasone suppression testing was performed on all patients. Plasma levels of cortisol were not significantly decreased after low-dose testing, but plasma levels of cortisol were significantly decreased after high-dose testing in the diffuse hyperplasia group. In summary, due to the pathological changes of the adrenal cortex, dexamethasone suppression testing can differentiate between the two types of Cushing's syndrome.

Adolescent↗
PubMed1977

[Functional morphology of the hypothalamo-hypophyseal neurosecretory system and adrenal cortex in myocardial infarct].

The hypothalamo-hypophyseal neurosecretory system (HHNS) was studied in patients dying at various intervals after the onset of the first clinical manifestations of myocardial infarction. All the 75 cases were divided into two groups depending on the presence or absence of decompensation with disorders of the water-salt metabolism. Despite the duration and pattern of its course, myocardial infarction was shown to be always accompanied by a high activity of the HHNS and adrenal cortex, although different variants of its intensity could be distinguished by the studies of the secretory cycle in neurosecretory nuclei. When infarction was complicated by cardiac decompensation, there developed the state of hypervasopressinism constantly accompanied by hyperthrophy of the glomerular zone of the adrenal cortex producing aldosteron and by an increased concentration of intracellular sodium.

Adrenal Cortex↗
PubMed1989

Differential effects of heparin on inositol 1,4,5-trisphosphate binding, metabolism, and calcium release activity in the bovine adrenal cortex.

In a wide variety of cells, inositol-1,4,5-triphosphate is a second messenger that interacts with specific intracellular receptors and triggers the release of sequestered Ca2+ from an intracellular store. We have looked at the influence of heparin on the action and metabolism of inositol-1,4,5-triphosphate in the bovine adrenal cortex. Heparin blocked inositol-1,4,5-trisphosphate binding with half-maximal efficiency around 10 micrograms/ml. Scatchard analyses revealed that heparin did not change the affinity but decreased the number of available binding sites. The Ca2+-releasing activity of inositol-1,4,5-trisphosphate was monitored with the fluorescent indicator, fura-2. Heparin blocked this activity with half-maximal effeciency around 10 micrograms/ml. The effect of heparin could be overcome by a supramaximal dose of inositol-1,4,5-trisphosphate (25 microM). The activity of inositol-1,4,5-trisphosphate-3-kinase from bovine adrenal cortex cytosol was also studied. Heparin inhibited the activity of the kinase with a half-maximal effeciency around 0.4 microgram/ml. Lineweaver-Burk plots revealed that this potent effect was noncompetitive. Finally, we observed that heparin is without effect on inositol-1,4,5-trisphosphate-5-phosphatase (at concentrations as high as 2 mg/ml). These results are consistent with the suggestion that the binding sites for inositol-1,4,5-trisphosphate are the intracellular receptors responsible for the Ca2+-mobilizing effects of inositol-1,4,5-trisphosphate. These results also show that the kinase, the phosphatase, and the receptor are three different molecular entities, which are affected in a different manner by heparin.

Adrenal Cortex↗
PubMed1998

Autoradiographic evidence that zona glomerulosa and capsular vessels of the human adrenal cortex are provided with different subtypes of adrenomedullin receptors.

Frozen sections of normal adrenal glands, obtained from patients undergoing unilateral nephrectomy for kidney cancer, were labeled in vitro with human [125I]ADM(1-52). Autoradiography and quantitative densitometry showed the presence of abundant ADM(1-52) binding sites in both zona glomerulosa (ZG) and capsular vessels, which were displaced with about the same efficiency by cold ADM(1-52) and rat ADM(1-50). The selective calcitonin gene-related peptide type 1 (CGRPI) ligand CGRP(8-37) eliminated, although less efficiently than ADMs, [125I]ADM(1-52) binding in the ZG, but not in the capsular vessels. These findings suggest the existence of different receptor subtypes for ADM in the human adrenal cortex. The CGRP(8-37)-sensitive receptors located in the ZG may mediate the well-known inhibitory effect of ADM on aldosterone secretion, while the CGRP(8-37)-insensitive receptors present in the capsular vessel may be involved in the ADM-induced rise in adrenal blood flow.

Adrenal Cortex↗