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PubMed2000

ACTH-regulated expression of vascular endothelial growth factor in the adult bovine adrenal cortex: a possible role in the maintenance of the microvasculature.

Endothelial cells lining vessels of endocrine tissues are fenestrated. Interactions with the local environment via either soluble factors or cell-cell interactions appear to govern this terminal endothelial differentiation. Adrenocorticotropin (ACTH) has previously been reported to modulate endothelial fenestration in the rat adrenal cortex. Since vascular endothelial growth factor (VEGF) has been characterized as a potent inducer of endothelial fenestration, we aimed to characterize the status of VEGF expression in the bovine adult adrenal cortex and asked whether ACTH may regulate VEGF expression. By immunohistochemical analysis, we observed VEGF expression in steroidogenic cells from both zona glomerulosa and zona fasciculata of the bovine adrenal cortex. Double-labeling experiments performed on isolated cells in primary culture revealed VEGF immunoreactivity, essentially colocalized with the Golgi apparatus. The expression of two predominant VEGF isoforms, VEGF(121) and VEGF(165), was observed by RT-PCR analysis. ACTH (10 nM) was found to rapidly (within 2-4 h) increase the abundance of these VEGF transcripts, as assessed by both RT-PCR and Northern blot analysis. In parallel, ACTH significantly induced VEGF secretion into the medium of fasciculata cells in primary culture. Thus, our data are consistent with the involvement of ACTH, through its regulation of VEGF expression, in the maintenance of the adult adrenal cortex endothelium.

Adrenal Cortex↗
PubMedDate not supplied

[Content of biological antioxidants and lipid peroxidation in the adrenal cortex in experimental circulatory insufficiency].

Thirteen-week experimental insufficiency in rats causes exhaustion of adrenal cortex function. The number of diene conjugates in the adrenals increased, the alpha-tocopherol level decreased. It is suggested that reduced level of antioxidant protection and the associated activation of lipid peroxidation processes underlie the disorders of adrenal cortex function.

Adrenal Cortex↗
PubMed1995

Role of the adrenal cortex and medulla in the young rats' glucoregulatory response to endotoxin.

The importance of the adrenal gland in the 10 day old (10 d) rats' glucoregulatory response to endotoxin (ETX) was investigated. Plasma glucose, lactate, and liver glycogen were measured at 0, 2, 3, and 4 h after ETX to 10 d adrenalectomized (ADRNX), adrenal demedullated (MEDX), and sham-operated (SHAM) rats. At 24 h after ETX, mortality in the ADRNX group was a striking 86% compared with 34% and 36% in intact and SHAM groups, respectively. Mortality in MEDX rats (47%) did not differ from control groups. Although MEDX exacerbated hypoglycemia at 3 and 4 h after ETX (p < or = .05), ADRNX produced severe hypoglycemia by 2 h after ETX. Lactacidemia occurred earlier and was greater in ADRNX rats than in MEDX and SHAM rats. Unlike MEDX, ADRNX significantly decreased liver glycogen and ETX rapidly depleted the remaining glycogen by 2 h after injection. These results demonstrate the greater importance of the adrenal cortex relative to the adrenal medulla in the 10 d rats' defense against ETX-induced hypoglycemia, hyperlactacidemia, and lethality.

Adrenal Cortex↗
PubMed1997

Adrenal cortex alterations in mice infected with Plasmodium berghei.

The ultrastructural study of adrenal cortex from Plasmodium berghei infected mice showed different degrees of capillary wall alterations including disruption and widening of the fenestrae, capillaries packed with parasitized erythrocytes, necrosis of cortical cells, parasitized erythrocytes outside capillaries and in some instances inside cortical cell cytoplasm. Lymphocytes were also observed in degenerated cortical cells. Our results suggest that adrenal cortex lesions may be relevant in the etiopathogenesis of severe malaria.

Adrenal Cortex↗
PubMed1993

Estrogen and hydroxysteroid sulfotransferases in guinea pig adrenal cortex: cellular and subcellular distributions.

This report describes for the first time the cellular and subcellular localization of estrogen sulfotransferase (EST) as well as the subcellular localization of hydroxysteroid sulfotransferase (HST) in the mammalian adrenal cortex. A 34-kilodalton EST and two HSTs with 3 alpha- and 3 beta-hydroxysteroid substrate specificities (32 and 33 kilodaltons, respectively) were previously purified from guinea pig adrenal cortex and characterized. Western blots were used to establish that two antisera generated against EST were highly specific for EST, whereas three antisera generated against the HSTs were highly specific for the HSTs, but did not distinguish between the 3 alpha- and 3 beta HSTs. Light and electron microscopic immunoperoxidase labeling with these antisera revealed that the sulfotransferases were expressed only within the ACTH-responsive layers of the guinea pig adrenal cortex, with EST localized to zona fasciculata and zona reticularis cells, and the HSTs confined to the zona reticularis. No labeling was detected in the zona glomerulosa or adrenal medulla. EST was concentrated in cell nuclei; sparse labeling was distributed throughout the cytoplasm. HST labeling was intense in smooth endoplasmic reticulum of zona reticularis cells, but was absent from nuclei. Ovoid inclusions about 1-4 microns in diameter, with no limiting membrane, were observed in zona reticularis cells; these inclusions were strongly labeled for both EST and HSTs. No gender-specific differences in distribution or labeling intensity were apparent. The high concentration of EST immunoreactivity in nuclei suggests that EST may play a role in modulating the ability of active estrogens to regulate gene expression in ACTH-responsive cells. The distribution of HST labeling suggests that sulfonation of adrenocortical 3-hydroxysteroids takes place largely within smooth endoplasmic reticulum in the zona reticularis in adult guinea pigs.

Adrenal Cortex↗
PubMed1988

Immunohistochemistry of cytochrome P-450 21-hydroxylase: microscopic examination of the enzyme in the bovine adrenal cortex and kidney.

Cytochrome P-450 specific for steroid 21-hydroxylase (P-450C21) localized in bovine adrenal cortex and kidney was immunocytochemically observed by the peroxidase-antiperoxidase method using a specific antibody. P-450C21 was present in all three zones of the adrenal cortex. Immunoreactivity for P-450C21 was intense in the zona glomerulosa and inner reticularis and faint in the area between the zona glomerulosa and outer fasciculata, probably representing the zona intermedia. The positive stain was only observed in parenchymal cells. The immunoreactivity varied within each zone, especially in the zona reticularis. In the kidney, immunoreactivity for P-450C21 was exclusively localized in the distal and cortical and medullary collecting tubules. This corresponds to the site of mineralocorticoid action in the kidney. No immunoreactivity was observed in the liver and aorta.

Adrenal Cortex↗
PubMed1981

[Connections between the mast cell system of a focus of inflammation and the zona fasciculata of the adrenal cortex].

At aseptic inflammation developing around a solid foreign body and proceeding both under common conditions and on the background of disturbed inactivation of free amines as a result of monoaminoxidase blockade with vetrasin or devastation of amine tissue depots with reserpine it has been stated that indices of the adrenal cortex activity (hyperemia, contents of ascorbic acid and corticoids) and those of the mast cells system in the inflammatory focus (amount of the cells, their size, contents of glycosaminoglycans, RNA, tryptophan and histidine) are subjected to certain fluctuations during inflammation. Increasing activity of the adrenal cortex fascicular zone and renewal of the mast cell population in the inflammatory focus are directly proportional to the degree of a disturbed deposition of free amines in the organism. Certain positive correlations prevail in cooperation of the adrenal cortex activity, decomposition rate of large (mature) mast cells and migration into the inflammatory focus of small (immature) forms of these cells.

Adrenal Cortex↗
PubMed1977

Effects of exogenous ACTH on the rat fetal adrenal cortex: a histochemical and electron-microscopical observation.

ACTH was administered subcutaneously to rat fetus directly at the late stage of fetal development and acute reaction on the fetal adrenal cortex was observed histochemically and electron microscopically. By administration of ACTH the adrenal cortex became remarkably hyperemic and there were swollen cells in all layers, particularly in the middle and inner layers (corresponding to the zona fasciculata and reticularis in adult rat). Marked reduction of lipid, enlarged mitochondria with increased vesicular cristae and increased smooth-surfaced endoplasmic reticulum (SER) were characteristic. The alterations of mitochondria preceded the change of SER, and thereafter mitochondria showed rapid degeneration. The outer layer (corresponding to the zona glomerulosa in adult rat) also showed similar changes by ACTH to those of the other two layers. These results indicated that the fetal adrenal cortex of rats was exogenous ACTH-reactive and its reaction which was different from that of adult cortical cells, seemed to be specifically related to the development and differentiation of the cells.

Adrenal Cortex↗
PubMed2003

[Clinical significance of the function of adrenal cortex in refractory congestive heart failure].

OBJECTIVE: To investigate the function of adrenal cortex in refractory congestive heart failure and to testify the hypothesis that glucocorticosteroid can improve the effectiveness of medicine on this disease. METHODS: Thirty-eight patients with refractory congestive heart failure (men 23 and women 15) were enrolled in this study and randomly divided into two groups, control group and treatment group. The cardiac index and ejection fraction were applied to evaluate the cardiac function and the level of blood cortisol was used to estimate the adrenal cortex function. RESULTS: The level of blood cortisol was low at the time of hospitalization in all studied patients. Moreover, the digoxin, diuretic and vasodilating had little effective ness in those patients. However, the glucocorticosteroid at a low dosage was able to improve the effectiveness of those medicines on congestive heart failure. The cardiac index, left ventricular ejection fraction and urine output dramatically increased after glucocorticosteroid treatment. There was a significant difference between the treatment group and control group (23.8 percent vs. 70.6 percent, P<0.01). In addition, the mortality in treatment group was also lower than that in control group (38.1 percent vs. 58.8 percent, P>0.05). CONCLUSION: Glucocorticosteroid at a low dosage obviously improved the effectiveness of medicines on congestive heart failure, and increased the survival rate in the patients.

Adrenal Cortex↗
PubMed1990

[Structural organization of the adrenal cortex in rats with different types of autonomic reactivity under standard conditions and after exposure to different altitudes].

The structural organization of adrenal cortex has been studied in intact rats and after short-term hypoxia exposure on different altitudes (2, 6, 8, 11 km). Previously rats have been divided into 3 groups by adrenaline test for determining of vegetative reactivity type. It has been found that some histochemical and morphometric indices of adrenal cortex had peculiarities with respect to type of vegetative reactivity (width of zones, their ratio, nuclear diameter, ascorbic acid content and its distribution and other) in intact rats. Under altitude these differences form individual character of steroidogenesis and determine resistance and reactivity of organism.

Adrenal Cortex↗
PubMed2002

Endothelin-1[1-31]: a novel autocrine-paracrine regulator of human adrenal cortex secretion and growth.

Endothelin (ET)-1[1-21] stimulates steroid secretion and zona glomerulosa growth and is expressed in the human and rat adrenal cortex together with its receptor subtypes A and B (ETA and ETB). Although ET-1[1-21] is generated from bigET-1 by an ET-converting enzyme (ECE-1), there is evidence of an alternative chymase-mediated biosynthetic pathway leading to the production of an ET-1[1-31] peptide, the role of which in adrenal pathophysiology is largely unknown. Gene expression and immunohistochemical studies allowed localization of chymase in the normal human adrenal cortex. Sizable amounts, not only of ET-1[1-21] but also of ET-1[1-31], were found in the adrenal vein plasma of three patients. ET-1[1-21] and ET-1[1-31] elicited a clear-cut secretory response by dispersed human adrenocortical cells, ET-1[1-31] being significantly less potent than ET-1[1-21]. The secretagogue effect of ET-1[1-31] was abolished by the ETA receptor antagonist BQ-123 and was unaffected by the ETB receptor antagonist BQ-788. Because, in humans, the secretagogue effect of ET-1[1-21] involves both ETA and ETB receptors, the weaker action of ET-1[1-31] could be attributable to a selective ETA receptor activation. Two lines of evidence support this contention: 1) ET-1[1-31] was more effective than ET-1[1-21] in stimulating ETA-mediated cell proliferation of human adrenocortical cells cultured in vitro; and 2) autoradiography showed that a) ET-1[1-31] displaced in vitro [(125)I]ET-1[1-21] binding to the ETA, but not ETB receptors, in human internal thoracic artery rings; and b) BQ-123, but not BQ-788, eliminated [(125)I]ET-1[1-31] binding in the rat adrenal cortex.

Adrenal Cortex↗
PubMed1962

Action of 1,1,dichloro-2-p-chlorophenyl-2-o-chlorophenylethane on dog adrenal cortex.

A single intravenous injection of op'DDD (1,1,dichloro-2-p-chlorophenyl-2-o-chlorophenylethane) has an acute effect on the adrenal cortex of the dog. Within 2 hours after intravenous injection of the drug, there is a decrease in the in vitro response of the adrenal cortex to stimulation by adrenocorticotrophic hormone and an inhibition of glucose-6-phosphate dehydrogenase activity. The inhibition of glucose-6-phosphate dehydrogenase activity might explain the effect of op'DDD on corticosteroid production.

Adrenal Cortex↗