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Results for “ADRENAL CORTEX”

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At least 703 records · Page 39Linked to original sources
PubMed1988

Effects of pH, reducing and alkylating reagents on the binding and Ca2+ release activities of inositol 1,4,5-triphosphate in the bovine adrenal cortex.

In a wide variety of cells, inositol 1,4,5-triphosphate (IP3) is a second messenger which interacts with specific intracellular receptors and triggers the release of sequestered Ca2+ from an intracellular store. When bovine adrenal cortex microsomes were incubated in the presence of dithiothreitol [(DTT) IC50 = 50 mM] or n-ethylmaleimide [(NEM) IC50 = 0.5 mM], they lost their IP3 binding capacity. Scatchard analysis of the binding data revealed that DTT decreased the affinity while NEM decreased the number of binding sites for IP3. The effect of DTT was reversible whereas the effect of NEM was permanent. pH variations between 6.5 and 9 increased the IP3 binding capacity of the microsomes. The effects of DTT, NEM, and pH on IP3-induced Ca2+ release from the microsomes were consistent with their effects on IP3 binding. Our data show that the binding sites for IP3 in the bovine adrenal cortex are proteins containing disulfide bridges and free sulfhydryl group(s) which are essential features for the recognition of IP3. These results also suggest that the binding sites for IP3 are the physiological receptors through which IP3 triggers the mobilization of Ca2+ in adrenal cortex in response to angiotensin II and other Ca2+ mobilizing ligands.

Adrenal Cortex↗
PubMed1997

Phosphoserine/threonine phosphatases in the rat adrenal cortex: a role in the control of steroidogenesis?

The involvement of protein kinases in the signal transduction pathways controlling adrenal steroidogenesis is well established, and the phosphorylation of substrates by cAMP-dependent protein kinase is a major mechanism in ACTH action. However, the possibility that protein phosphatases (PPs) might also be involved in this process has not been investigated. The aim of this study was, therefore, to measure the function, expression and enzymic activity of PPs in zona glomerulosa (ZG) and zona fasciculata/reticularis (ZFR) tissue from the rat adrenal cortex. Immunoblot analysis using specific antisera demonstrated the presence in whole adrenals and capsules of PP type 1 (PP1) migrating with an apparent molecular mass of 37 kDa, and PP type 2A (PP2A) migrating with apparent molecular masses of 38 and 31 kDa. The PP inhibitors, okadaic acid (OA), calyculin A (CA), tautomycin and microcystin RR, caused a reduction in PP activity in vitro, at doses between 1 nM and 1 microM. In addition, treatment of ZG cells with the adenylate cyclase stimulator, forskolin (10 microM) resulted in a significant reduction in PP activity. The effects of CA and OA on steroid secretion by ZG and ZFR cells were also investigated. Neither CA nor OA had any effect on basal steroid secretion or on yields of steroid obtained from 22R-hydroxycholesterol at doses between 1 and 100 nM. However, both OA and CA (10 and 100 nM respectively) significantly reduced ACTH-stimulated aldosterone and corticosterone production by ZG and ZFR cells. CA and OA (10 and 100 nM respectively) also reduced steroid secretion by cells stimulated by forskolin (10 microM) or dibutyryl cAMP (200 microM). These results suggest that PPs may be involved in the intracellular mechanisms through which adrenocortical steroidogenesis is regulated, acting at a point after cAMP generation and action, but proximal to the side-chain cleavage of cholesterol.

Adrenal Cortex↗
PubMed1988

Aldosterone biosynthesis in mitochondria of isolated zones of adrenal cortex.

An assumption that the aldosterone-synthesizing enzyme exists only in zona glomerulosa cells apparently contradicts our recent findings that a purified bovine adrenocortical cytochrome P-45011 beta catalyzes the aldosterone formation and the enzyme exists in both zones of the adrenal cortex. To gain more insight into the zone specificity of aldosterone production, the aldosterone-synthesizing activity of mitochondria prepared from the isolated zones of adrenal cortex of various animal species was investigated. The intact mitochondria from the bovine or porcine zonae fasciculata-reticularis could not produce aldosterone whereas those from the zona glomerulosa produced it at a significant rate. When the mitochondria from the zonae fasciculata-reticularis were solubilized by the addition of cholate, they produced aldosterone from corticosterone at a rate comparable to that of those from the zona glomerulosa. The presence of specific factor(s) in the zonae fasciculata-reticularis mitochondria inhibiting expression of the aldosterone synthetic activity is discussed. The mitochondria of the rat zonae fasciculata-reticularis could hardly catalyze aldosterone synthesis under the detergent-solubilized conditions, whereas those of the zona glomerulosa could. Immunoblot analysis revealed that the mitochondria of the zonae fasciculata-reticularis contained a protein of Mr 51,000 which was immunocrossreactive with a monoclonal antibody directed against P-45011 beta, whereas those of the zona glomerulosa contained two immunocrossreactive proteins of Mr 51,000 and 49,000. These results suggest that in the case of rat adrenal cortex, a specific aldosterone-synthesizing enzyme exists in the zona glomerulosa.

18-Hydroxycorticosterone↗
PubMed1987

Direct stimulation of the adrenal cortex by interleukin-1.

The impact of human recombinant beta-interleukin-1 (IL-1) on adrenocortical stimulation was investigated. This study asked three questions: Does IL-1 increase the corticosterone levels of rat serum? Is there a direct effect on the adrenal cortex? What is the mechanism of this effect? The intraperitoneal injection of IL-1 (70 micrograms) in anesthetized male Fisher rats resulted in elevated corticosterone levels at 30 minutes and reached a maximum at 180 minutes (94 +/- 12 versus 34 +/- 4 micrograms/dl, p less than 0.01). Next, the adrenal glands from separate animals were perfused in situ. Corticosterone secretion was significantly increased (p less than 0.01) 90 minutes after a single arterial bolus of 35 micrograms of IL-1. The response to IL-1 was dose dependent, beginning at 3.5 micrograms and reaching a maximum at 35 micrograms. The addition of indomethacin (3 mumol/L) completely abolished the stimulatory effect of IL-1. This study demonstrates that IL-1 increases rat serum corticosterone levels, IL-1 directly stimulates the adrenal cortex, and the stimulation may be mediated through prostaglandin synthesis. This is the first evidence that IL-1 has a direct stimulatory effect on the adrenal cortex.

Adrenal Cortex↗
PubMed1998

Iatrogenic Adrenal Cortex Failure in Patients with Steroid Dependent Asthma in Relation to Different Methods of Glucocorticoid Treatment.

OBJECTIVE: To evaluate and compare the degree of adrenal cortex suppression in patients receiving long term treatment with different formulas and doses of glucocorticoids (GC) which is of considerable diagnostic and therapeutic importance. METHODS: A total of 97 subjects (51 women and 46 men) with bronchial asthma was divided into the groups subjected to different GC treatment (e.g. inhalation, oral and intramuscular GC). In all patients total blood serum and free salivary cortisol was estimated under basal conditions and after Synacthen stimulation as well as free cortisol and its metabolites in 24 hour urine. RESULTS: Reduced adrenal reserve was found in 58.33 % of patients chronically treated with systemic GC, in 21.05 % of patients periodically treated with systemic GC and in 9.09 % of patients treated with inhaled GC. CONCLUSIONS: Inhaled GC caused a small degree of adrenal cortex suppression and thus should be preferred in the treatment of bronchial asthma. In addition, free salivary and urinary cortisol levels are a useful non-invasive method of evaluating adrenal cortex function in patients with bronchial asthma.

Journal Article↗
PubMed1973

Fine structure and morphogenesis of spironolactone bodies in the zona glomerulosa of the human adrenal cortex.

Numerous spironolactone bodies have been detected in the zona glomerulosa cells of the adrenal cortex of a 36-year-old spironolactone-treated woman whose non-tumorous right adrenal gland was removed surgically because of primary hyperaldosteronism. Electron microscopy revealed spherical laminated whorls which consisted of a central core composed of an amorphous electron-dense material surrounded by numerous smooth-walled concentric membranes. Continuous with and deriving from the endoplasmic reticulum, they were present in viable cells and were not associated with ultrastructural features indicating cellular injury. Cytoplasmic inclusions similar to spironolactone bodies can be detected in other organs after the administration of various compounds. Thus, they can be regarded as neither specific to spironolactone treatment nor exclusively inducible in the zona glomerulosa of the adrenal cortex.

Adrenal Glands↗
PubMed1977

[Several indices of the functional state of the pituitary--adrenal cortex system in chronic alcoholism].

The adrenal cortex functional activity in males with alcoholsim of the 2nd stage (128 cases) in respect to the production of glucocorticoids and mineral-corticoids is decreased. The biosynthesis of androgens, as can be seen by the 17-KS urine excretion, is increased. Abstinence from alcohol during treatment with teturam in combination with neuroleptical drugs was accompanied by an increased elimination of glucocorticoids and a normalization of the metabolic indices of the main electrolytes. In all the examined cases of alcoholism with the 2nd stage irrespective of the duration of the disease there was an increased amount of androgens, possibly as a compensatory reaction to metabolic disturbances, due to chronic alcoholic intoxication.

17-Hydroxycorticosteroids↗
PubMed2000

Effects of recombinant murine leptin[1-147] and leptin fragment 116-130 on steroid secretion and proliferative activity of the regenerating rat adrenal cortex.

Leptin, the product of the ob gene, is a hormone mainly secreted by the adipose tissue, which acts through specific receptors (Ob-R) widely distributed in the body tissues. Ob-Rs are present in the mammalian hypothalamo-pituitary-adrenal axis, and evidence indicates that leptin regulates adrenocortical secretion. Moreover, leptin is known to act as a growth promoting factor in some tissues, including the endocrine ovary. We have investigated the effects of three subcutaneous injections of 2 nmol/100 g of native murine leptin[1-147] and of its biologically active fragment 116-130 on the secretory and proliferative activity of the regenerating rat adrenal cortex. Leptin[1-147] increased plasma aldosterone concentration at day 8 and plasma corticosterone concentration (PBC) at day 5 of regeneration, without affecting mitotic index. In contrast, leptin[116-130] lowered PBC and mitotic index at both times of adrenal regeneration. In light of the fact that adrenal regeneration is at least in part dependent on the pituitary ACTH, we conclude that: (i) native leptin moderately stimulates steroid secretion, acting directly on the adrenal cortex, through signaling mechanisms other than those involved in the ACTH action; (ii) native leptin is unable to enhance the proliferative activity of regenerating adrenals, which conceivably is maximally stimulated by ACTH; (iii)leptin[1-147] and leptin[116-130] differently interact with Ob-Rs or interact with different receptors; and (iv) leptin[116-130] inhibits the signaling pathways mediating both the secretagogue effect of native leptin and the proliferogenic effect of ACTH.

Adrenal Cortex↗