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At least 1,207 records · Page 67Linked to original sources
PubMed1986

Low-density lipoprotein receptor activity in the guinea pig adrenal cortex. II. Zonal response to aminoglutethimide and 17 alpha-ethinylestradiol.

Low-density lipoprotein (LDL) receptor activity and the concentration of cholesterol were measured in the outer (glomerulosa/fasciculata) and inner (reticularis) zones of the adrenal cortex of the guinea pig to examine the relation between cholesterol content and LDL receptor activity. While the concentration of cholesterol was 2-3-times higher in the outer cortical zone, the maximum high-affinity binding capacity for LDL was essentially the same for the two zones, or slightly higher for the inner zone. Adrenocorticotrophic hormone (ACTH) caused a significant increase in LDL receptor activity only in the outer zone, but led to a reduction in the cholesterol content in both adrenocortical zones. The treatment of animals with 17 alpha-ethinyl-estradiol also resulted in a reduction of cholesterol in both adrenocortical zones, but an increase in LDL receptor number only in the outer zone. The latter effect was partially reversed by the administration of dexamethasone. Aminoglutethimide, which was used in a dose that did not block steroidogenesis but did block the hydrolysis of cholesteryl esters in response to ACTH, did not prevent the ACTH-induced increase in LDL receptor number in the outer zone. Thus, the number of LDL receptors was increased in the zona fasciculata by ACTH in the absence of a reduction in cellular cholesterol content, while the number of LDL receptors in the zona reticularis was not increased by ACTH even in the face of a reduction in cellular cholesterol. Exclusive of the experiments employing aminoglutethimide, when the cellular cholesterol content was plotted against LDL binding activity, an excellent inverse correlation was revealed for the zona fasciculata, but essentially no correlation was noted for the zona reticularis. It is concluded that the outer and inner cortical zones of the guinea pig adrenal are quite distinct in the nature of their LDL receptor activity and regulation: the LDL receptor of the outer zone appears to function in a way similar to what has been reported for the whole adrenal cortex of other species in that receptor number correlates with tissue cholesterol content and is primarily regulated by ACTH; the LDL receptor number of the inner zone, however, does not correlate with tissue cholesterol content and is apparently not regulated by ACTH.

Adrenal Cortex↗
PubMed1982

Response of the adrenal cortex to tetracosactrin (ACTH1-24) in the premature and full-term foal.

The changes in plasma cortisol concentration in the immediate postnatal period were examined in 3 groups of newborn foals and the response of the adrenal cortex to exogenous ACTH1-24 (tetracosactrin) was tested in 2 of these groups. In full-term Thoroughbred and Pony foals a rise in plasma cortisol occurred between 0 and 30 min after birth, whereas no significant cortisol changes could be detected within 2 h of birth in the group of prematurely delivered foals. These differences in plasma cortisol between term and premature foals were accompanied by differences in blood pH and lymphocyte and neutrophil counts. The high cortisol concentrations in the term animals declined to low levels by 4-12 h after birth. There was also a clear distinction between the responsiveness of the adrenal cortex to ACTH in the term and premature animals. When short-acting tetracosactrin was given as a single i.m. injection (0.125 mg), a rapid rise in plasma cortisol occurred in all term foals whereas no response was detected in the premature group during the same 2-h test period. The adrenal cortical response was also accompanied by a significant fall in the neutrophil/lymphocyte ratio at 2 h after the injection; no such change was seen in the premature animals. After a 24-h period of treatment with depot tetracosactrin (3 doses; 0.4, 0.2, 0.2 mg i.m.), a 2nd test with short-acting tetracosactrin led to a rise in plasma cortisol in term and pre-term foals during the 2-h test period. The depot tetracosactrin also appeared to cause a 3-fold increase in basal plasma cortisol levels in both groups.

Adrenal Cortex↗
PubMed1999

Radionuclide imaging of the adrenal cortex.

Adrenocortical scintigraphy provides information concerning cortical function that is not readily available by other means. The ability to map differential adrenal cortical function has great clinical utility and demonstrable cost-effectiveness in the evaluation of adrenocortical disease and in distinguishing benign from malignant lesions in patients with incidentally discovered adrenal masses.

Adrenal Cortex↗
PubMed1990

Regulation of the primate fetal adrenal cortex.

Significant advances in our understanding of the regulation of fetal adrenal growth, differentiation, and steroidogenesis have been made in the past several years. In vitro studies employing molecular biological techniques have demonstrated that the placenta and several fetal tissues synthesize growth factors and/or oncogene-related products, which have the capacity to modulate growth and maturation of the fetal adrenal. Moreover, there is evidence that the fetal adrenal itself produces IGF-I and IGF-II and that the mRNAs for these growth factors are responsive to ACTH and perhaps other peptides originating in the fetal pituitary and/or the placenta. Most fascinating are the studies demonstrating that growth factors may also regulate the pattern of steroidogenesis elicited by the fetal adrenal. For example, TGF beta modulates binding, internalization, and degradation of LDL-cholesterol in adult adrenals while IGF-I increases fetal adrenal steroidogenesis by mechanisms that do not involve induction of P-450scc or enhanced metabolism of LDL. These studies, coupled with the observation that activation of protein kinase C by EGF or bFGF can block ACTH and/or other cAMP-induced increases in the activity of P-450(17 alpha), provide new insight into the subcellular mechanisms that underlie the regulation of fetal adrenal function. However, in vivo investigations must be aggressively pursued because the latter provide a major and perhaps exclusive means to elucidate the complex and multiple mechanisms that are apparently operative in utero in the regulation of fetal adrenal development. Moreover, in vivo studies remain the only valid means to delineate whether the factors that have been shown to modulate fetal adrenal function in vitro are indeed operable in vivo. Thus, in vivo investigations have shown that a multifactorial regulation of the fetal adrenal exists in utero in which PRL and perhaps other peptides as well as ACTH selectively stimulate fetal adrenal androgen production. Moreover, in vivo studies have demonstrated that a feedback mechanism operates in utero whereby estrogen produced in the placenta from androgen precursors of fetal adrenal origin feeds back to modulate the responsivity of the fetal adrenal to tropic peptides perhaps by regulating peptide binding to cell membrane receptors and/or other mechanisms. Evidence has also been provided from in vivo studies to support the concept that the placenta via metabolism of maternal cortisol and cortisone regulates fetal pituitary production of ACTH by modulating the extent to which maternal cortisol arrives at the fetus.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex↗
PubMedDate not supplied

Zonation, paracrine function and aldosterone secretion in the rat adrenal cortex.

Using in situ hybridisation we show that, in the rat adrenal, 11 beta-hydroxylase is confined to the inner zones, whereas aldosterone synthase is expressed exclusively in the glomerulosa. Immunoblotting methods identify an 18-hydroxydeoxycorticosterone (18-OH-DOC) in IEF gels of solubilised inner adrenocortical zone membrane preparations. This steroid, which can also be identified by immunocytochemistry, cannot be solvent extracted from the IEF gels unless the gel slices are first treated with trypsin. Preincubation of viable whole glandular tissue with trypsin significantly enhances aldosterone output, and eliminates the trypsin releasable 18-OH-DOC pool in IEF gels. The data suggest that 18-OH-DOC is synthesised and sequestered in inner zone cells, in a novel non-solvent extractable manner, but can be mobilised for utilisation as an aldosterone precursor in the glomerulosa.

Adrenal Cortex↗
PubMed1981

Effect of 4-cholesten-3-one on steroidogenesis and morphology of rat adrenal cortex.

The production of corticosteroids from endogenous precursors was decreased in adrenal glands of male rats fed a diet containing one per cent of 4-cholesten-3-one for 3 and 7 days. In contrast, the conversion of labelled progesterone into corticosteroids was only slightly affected as shown by the increased aldosterone to 18-hydroxydeoxycorticosterone ratio. Morphological method revealed lipoid adrenal hyperplasia developing progressively during the observation period. In the adrenal gland, the content of 4-cholesten-3-one rose slightly and, as shown in the experiment with labelled 4-cholesten-3-one, it can serve only as a weakly effective precursor of corticosteroid biosynthesis. Cholesterol content in the adrenals decreased and lipoid hyperplasia could not be explained therefore by cholesterol accumulation.

Adrenal Cortex↗
PubMed1985

Sex differences in adrenocortical structure and function. XIX. Differences in the compensatory hypertrophy of the adrenal cortex of the male and female hamster after unilateral adrenalectomy.

Stereological studies on the adrenal cortex of unilaterally adrenalectomised hamsters have revealed differences in adrenal compensatory hypertrophy in male and female animals. The operation evokes an increase in the average volume of the zona fasciculata cells in the male and of the zona reticularis cells in the female.

Adrenal Cortex↗
PubMed1982

Inactivation of delta5-3-ketosteroid isomerase(s) from beef adrenal cortex by beta, gamma-acetylenic ketosteroids.

The beta, gamma-acetylenic ketosteroids, 5-10-seco-19-norpregn-5-yne-3,-10,20-trione approximately 1 and 5,10-secoestr-5-yne-3,10,17-trione approximately 2 irreversibly inactivate both the C19-and the C21-delta 5-3-ketosteroid isomerase activities of beef adrenal cortex microsomes. At saturating concentrations of inhibitor half-lives of these enzyme activities vary from 45 to 240 s. It is uncertain whether the enzyme generates its own alkylating agent by isomerizing compounds approximately 3 and approximately 4 to the corresponding allenic ketones, namely (4R)-5,10-seco-19-norpregn-4,5-diene-3,10,20-trione approximately 3 and (4R)-5,10-secoestra-4,5-diene-3,10,17-trione approximately 4 since these are formed spontaneously in the buffer used to stabilize enzyme activity. In the presence of catalytic quantities of adrenal enzyme compound approximately 4 is a powerful competitive inhibitor for both 5-androstene-3,17-dione (Ki 8.0 microM) and 5-pregnene-3,20-dione (Ki 3.5 microM) indicating that the eventual alkylating event is active site-directed. The differences in Ki values and half-lives for inactivation support the view that the C19- and C21-delta 5-3-ketosteroid isomerase activities do not reside at the same catalytic site in beef adrenal cortex microsomes.

Adrenal Cortex↗
PubMed1975

[Changes in the glucocorticoid function of the adrenal cortex in patients with myocardial infarct treated with trioxazine and aminazine].

A protracted observation over the glucocorticoid function of the adrenal gland in patients with myocardial infarction educed a biphasic nature of changes in the concentration of the plasma and urine corticosteroids in this affection. Most informative are shown to be the evidences of activation of the hypothalamo-hypophysial-adrenal system furnished by the biologically active 11-oxycorticosteroids in the peripheral blood plasma. Psychopharmacological drugs produced a less intensive activation of the glucocorticoid function of the adrenal cortex in the acute period of myocardial infarction and they smooth down a renewed rise in the level of steroid during the subacute period of the disease. Chlorpromazine displays a stronger antistress action than does trioxazine, but the available data justify recommending both these drugs for the treatment of patients with myocardial infarction.

11-Hydroxycorticosteroids↗
PubMed1982

Dynamic structure of bovine adrenal cortex microsomal membranes studied by time-resolved fluorescence anisotropy of all-trans-1,6-diphenyl-1,3,5-hexatriene.

The motional properties of all-trans-1,6-diphenyl-1,3,5-hexatriene embedded in the microsomal membranes and in extracted lipid liposomes from bovine adrenal cortex are studied by fluorescence anisotropy decay measurements. The results demonstrate the existence of a nonvanishing value of the anisotropy (r infinity) in both systems. The r infinity values are significantly higher in the total membranes than in the protein-depleted liposomes, following the trend of the steady state anisotropy values previously reported (Gallay, J., Vincent, M., de Paillerets, C., Rogard, M., and Alfsen, A. (1981) J. Biol. Chem. 256, 1235-1241). This indicates that the depolarizing rotations of the probe are more restricted in the presence of proteins. No detectable effect of proteins on the reorientational correlation time can be observed. The temperature dependence of r infinity is not similar in both systems. In the complete membranes, a sharp decrease of r infinity value takes place between 27 and 32 degrees C, corresponding to 1/3 of the total curve of r infinity versus temperature is translated to lower temperatures. Thermal dependence of the reorientational correlation time is essentially the same in lipids and in complete membranes with an activation energy of 5 kcal mol-1. The results suggest that proteins play an essential role in organizing the deepest lipid region in the microsomal membranes from bovine adrenal cortex.

Adrenal Cortex↗
PubMed2004

Effects of leptin and leptin fragments on steroid secretion and proliferative activity of regenerating rat adrenal cortex.

Leptin, an adipose tissue-secreted hormone, acts via several isoforms of specific receptors (Ob-Rs), which may variously interact with the native leptin molecule and its fragments. Evidence has been provided that leptin affects rat adrenal functions, but the results were rather conflicting depending on the experimental condition examined (e.g. regenerating vs. mature or immature adrenal gland). Hence, we investigated the effects of three subcutaneous injections of murine leptin(1-147) and several leptin fragments (3 nmol/100 g body weight; 28, 16 and 4 h before the sacrifice) on the secretory activity and growth of regenerating rat adrenal cortex. The following leptin fragments were tested: murine leptin(116-130), and human leptin fragments 150-167, 138-167, 93-105, 22-56 and [Tyr]26-39. Leptin(1-147) enhanced plasma concentration of both aldosterone and corticosterone. The blood level of aldosterone was raised by leptin(116-130), leptin(138-167) and leptin(93-105), and that of corticosterone by leptin(93-105) and Tyr-leptin(26-39). Metaphase index (stachmokinetic method with vincristine) was unaffected by leptin(1-147), and lowered by leptin(116-130), leptin(150-167) and leptin(138-167). Collectively, our findings allow us to conclude that leptin and leptin fragments enhance the secretory activity and inhibit the growth of regenerating rat adrenal cortex, the biological activity of leptin being located in the C-terminal segment of its molecule.

Adrenal Cortex↗
PubMed1997

Selective expression of HSP70-1 gene in the adrenal cortex but not in the medulla of thermally stressed rats.

The heat shock protein 70 (HSP70) gene expression in rat adrenal glands was investigated. In situ hybridization and Northern blotting revealed a marked increase of inducible HSP70 (HSP70-1) gene expression in the adrenal cortex, but not in the medulla, after whole body hyperthermia. In vivo footprinting assay of HSP70-1 promoter region suggested a possible involvement of other factor(s) in addition to the heat shock factor (HSF). We also detected significant increases of both ACTH and corticosterone in the plasma of the hyperthermic rats. These results suggested some physiological factors other than HSF may also participate in the tissue-specific induction of HSP70-1 gene in vivo.

Adrenal Cortex↗