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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Explants prepared from the neocortex and the fetal zone of the human fetal adrenal (gestational age 13 to 18weeks) were maintained under conditions of organ culture for 7 to 9 days during which time they were exposed to hACTH and various related peptides. Corticotrophic activity was monitored by the daily release of dehydroepiandrosterone sulfate (3beta-hydroxy-5-androsten-17-one, 3-sulfate; DHA-S) and cortisol as quantified by radioimmunoassay, hACTH (2.2 x 10(-9) - 2.2 x 10(-8)M) was the most active in sustaining steroidogenesis by both neocortical and fetocortical cells. alpha-MSH possessed similar properties but not at concentrations lower than 10(-6)M, whereas CLIP (4.4 x 10(-9) - 1.1 x 10(-7)M), the 18-39 C-terminal moiety of ACTH, was devoid of activity. Corticotrophic activity with respect to fetocortical explants appeared to be that of maintenance of function best illustrated by dehydroepiandrosterone sulfate biosynthesis, while enhancement of steroidogenesis was observed in the neocortex as manifested by cortisol release. Although not eliminating the possible existence of a specific fetal corticotrophin related to ACTH1-39, the data indicate that hACTH is capable of regulating steroidogenesis in the fetal zone which is primarily geared to the formation of dehydroepiandrosterone sulfate.
Steroids 1978 Apr
PMID:Steroidogenic activity of hACTH and related peptides on the human neocortex and fetal adrenal cortex in organ culture. 20

The sources of cholesterol for steroid hormone production were examined using bovine adrenocortical (BAC) cells in primary culture. The experiments were designed to determine the effects of lipoproteins on cortisol production and the level of BAC cell 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Most studies on BAC cell lipoprotein requirements have been conducted using human low-density lipoprotein (hHDL); none have used the homologous bovine lipoproteins. BAC cells treated with corticotropin (ACTH) in a medium devoid of lipoproteins increased and maintained cortisol production 7- to 20-fold above basal levels. Under such conditions ACTH also increased the rate of HMG-CoA reductase activity. Inhibition of HMG-CoA reductase with mevinolin inhibited cortisol production by 85%, indicating that the cells were using cholesterol synthesized de novo for steroid production. Cortisol production was increased almost 40-fold above basal levels if hLDL (100 micrograms/ml) was included in the incubation medium. Human LDL also suppressed the levels of HMG-CoA reductase in a concentration-dependent fashion. Human HDL was without effect on either BAC cell steroidogenesis of HMG-CoA reductase. Addition of bovine LDL (bLDL) to the incubation medium also caused an increase in cortisol production and inhibited cholesterol synthesis. By contrast to hHDL, bHDL (100 micrograms/ml) increased the ability of BAC cells to produce cortisol production. Bovine HDL (bHDL) also was able to decrease HMG-CoA reductase, but not to the extent caused by hLDL or bLDL. These data demonstrate that bovine adrenal cells can use bHDL as a source of cholesterol for steroid hormone production. These findings may be of particular importance when one considers that in vivo, the bHDL content of bovine serum greatly surpasses the level of bLDL.
Steroids 1992 Apr
PMID:The role of bovine lipoproteins in the regulation of steroidogenesis and HMG-CoA reductase in bovine adrenocortical cells. 132 89

The concentrations of C-19 steroids were measured in guinea pig and rat adrenals before and after castration as well as after stimulation with adrenocorticotropin hormone (ACTH). Characterization of adrenal C-19 steroids was also carried out by isolation with high-performance liquid chromatography and gas chromatography/mass spectrometry (GC/MS). From radioimmunoassay (RIA) data, androstenedione (4-DIONE) and 11 beta hydroxyandrostenedione (11 beta-DIONE) were the major C-19 steroids found in guinea pig adrenals, and castration induced a decrease of 4-DIONE levels only while all other C-19 steroids remained unchanged. In rat adrenals, the major C-19 steroids were 4-DIONE and testosterone, and they were also markedly inhibited after castration. With the exception of 11 beta-DIONE, all other C-19 steroids in circulation were eliminated after castration in both animals species. After ACTH administration in the guinea pig, adrenal 4-DIONE and 11 beta-DIONE levels were markedly stimulated, while an increase of only 11 beta-DIONE was observed in plasma. In the rat, ACTH had a small stimulatory effect on adrenal 52-androstane-3 alpha, 17 beta-diol (3 alpha-DIOL) and plasma 11 beta-DIONE levels. Analysis of guinea pig adrenal steroids by GC/MS confirmed the presence of C-19 steroids in adrenals (namely, 4-DIONE and 11 beta-DIONE) while, in the rat, this could not be confirmed. Our data indicate that production of C-19 steroids occurs in guinea pig adrenals, and 11 beta-DIONE is the major C-19 steroid as well as the only C-19 steroid secreted into the circulation. In the rat, the production of C-19 steroids detected by RIA is not supported by GC/MS data.
Steroids 1990 Aug
PMID:Production and secretion of C-19 steroids by rat and guinea pig adrenals. 217 70

The effect of bromocriptine on the morphological picture and steroid content of the adrenal gland, and on certain pro-opiomelanocortin (C) peptides in the pituitary gland was evaluated in preadrenarchal rabbits. Eighteen immature male rabbits (5 weeks of age), were treated for 10 days with saline (n = 10,2 ml sc) or bromocriptine mesylate (n = 8, 3 mg/kg sc) two times/day. After the last administration all animals received dexamethasone (0.25 mg im) and the next morning, 60 min after ACTH injection (0.25 mg im), plasma was drawn and they were sacrificed. Adrenals and pituitaries were immediately removed. For each animal, one adrenal gland was fixed, dehydrated and embedded in paraffin for histology; the other one was stored in saline for determination of androstenedione (A), dehydroepiandrosterone (DHA), 17-OH progesterone (17 P), and cortisol. Steroids were analyzed by RIA after previous extraction and celite-ethyleneglycol chromatography, or directly (cortisol). The immunoreactivities (ir) related to beta-Endorphin (B-EP), ACTH and alpha-MSH were evaluated in pituitary homogenates using specific RIAs. The bromocriptine-treated rabbits showed a significant increase in the percentage of the adrenal zona reticularis (21.5 +/- 3.9% of total cortex vs. 12.7 +/- 1.3% in controls, p less than 0.05, mean +/- SE), and a decrease of the zona fasciculata (57.6 +/- 3.13% vs. 67.7 +/- 2.05% in controls, p less than 0.05). No significant changes were observed in the relative percentage of the zona glomerulosa.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of bromocriptine on pituitary and adrenal cortex in pre-adrenarchal rabbits. 254 67

Cholesterol, pregnenolone, progesterone, 11-deoxycorticosterone (11-DOC) and corticosterone were quantitated in subcellular fractions isolated from in vivo adrenocorticotropin (ACTH)-stimulated rat adrenal zona fasciculata/reticularis. Six adrenal subcellular fractions separated by discontinuous sucrose gradient centrifugation (lipid, 0.125 M sucrose, cytosolic, microsomal, mitochondrial and nuclear) were extracted with alkaline ether/ethanol and assayed by high pressure liquid chromatography (HPLC). Lipid fractions contained the major cholesterol stores, while most pregnenolone and progesterone was found in lipid, microsomal and mitochondrial fractions. The 0.125 M sucrose and cytosol fractions together contained approximately 75% of the total 11-DOC and corticosterone. The five steroids were only present in small amounts in organelle fractions containing steroidogenic enzymes. Homogenate and lipid fraction cholesterol decreased between 10 and 15 min and again 30 min after ACTH injection. In the homogenate, lipid, microsomal and mitochondrial fractions, pregnenolone and progesterone were increased after ACTH injection; peak pregnenolone and progesterone concentrations were often measured in adrenal gland sucrose, cytosolic, microsomal and mitochondrial fractions 15 to 20 min after rats were injected with ACTH. Although ACTH increased 11-DOC and corticosterone in all but the mitochondrial and nuclear fractions, the sucrose, cytosolic and microsomal 11-DOC, and cytosolic corticosterone increased most dramatically. In many fractions, peak 11-DOC and corticosterone concentrations were most often observed between the 10 and 15 min periods and again at 30 min.
Steroids
PMID:Extraction of corticosterone from cell homogenates and subcellular fractions of the rat adrenal cortex. III. ACTH-induced temporal subcellular redistributions of steroid precursors to corticosterone. 301 51

Potentiated pituitary-adrenocortical responses to the second of two identical small hemorrhages, spaced 24 h apart, are seen in the pentobarbital sodium-anesthetized dog. To investigate the role of pentobarbital anesthesia in these results and to better define the range of the effect, we studied awake trained dogs with chronic adrenal venous catheters. Each dog was bled an amount between 8.7 and 21.8% of measured blood volume [131I] (MBV) over 3 min, and peripheral and adrenal blood were sampled. Blood was reinfused 1 h later, and the dogs were fed. The same hemorrhage and experimental protocol were repeated 24 h later. Steroids were assayed by high-performance liquid chromatography-ultraviolet (HPLC-UV) and adrenocorticotropic hormone (ACTH) by radioimmunoassay (RIA). Secretory rates of cortisol were calculated using measured adrenal blood flow rates. Maximal secretion of cortisol was determined after injection of 100 mU ACTH following each experiment. Dogs whose day 1 cortisol secretion after hemorrhage was submaximal (hem volume = 14.8 +/- 3.7% MBV; n = 7) showed a greater cortisol secretory response to the same hemorrhage on day 2 (P less than 0.005). This increased cortisol response on day 2 was accompanied by an increased ACTH presentation rate (APR) (P less than 0.025) and by increased adrenal sensitivity to ACTH (P less than 0.025). The increased APR was caused by both an increased venous ACTH and by an increased adrenal blood flow. If posthemorrhage cortisol secretion was maximal on day 1, ACTH, APR, and ABF were not different on the 2 days. No hemodynamic differences were seen to explain these findings. These results confirm and extend our previous results.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary-adrenal responses to repeated small hemorrhage in conscious dogs. 302 12

To investigate the chronic effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on aldosterone secretion, synthetic alpha-MSH (8 micrograms/day) was infused in Sprague-Dawley rats by miniosmotic pumps for 5 days. Saline was infused in equivalent volume for 5 days using the same type of pumps in the control group of rats. Aldosterone secretion from the capsular cells of the two groups was examined in the basal state and in response to various stimuli of aldosterone secretion. Aldosterone secretion in vitro from the alpha-MSH-treated rats was significantly impaired in response to all stimuli tested including cyclic AMP, suggesting an intracellular defect in aldosterone synthesis in that group. These results are similar to those observed after chronic adrenocorticotropin administration.
Steroids
PMID:Impaired aldosterone secretion from dispersed adrenal capsular cells of chronically alpha-MSH-treated rats. 303 59

To determine whether a change in microsomal proteins can be correlated with adrenocorticotropic hormone (ACTH)-stimulation of rabbit adrenal 17 alpha-hydroxylase activity, rabbit adrenal microsomes were subjected to electrophoresis on polyacrylamide gels in the presence of sodium dodecylsulfate. Microsomes were obtained from rabbits stimulated with ACTH for 0, 2, 4, and 6 days. A protein band with a molecular weight of 53,000 was found to increase 31.1, 27.2 and 61.0 percent in 2-, 4-, and 6-day ACTH-stimulated microsomes as compared to controls; but 17 alpha-hydroxylase activity showed no apparent correlation, increasing 5-6 fold in all experiments. No new protein bands were found after ACTH stimulation, and no other changes in microsomal protein electrophoretic patterns after ACTH stimulation were found to correlate with the increases in 17 alpha-hydroxylase activity. The specific activity (nmol/mg protein) of cytochrome P-450 remained nearly the same throughout the stimulation periods. Tetramethylbenzidine staining for heme prosthetic groups on the electrophoretic gels displayed bands with molecular weights of 61,000, 58,000 and 53,000.
Steroids 1984 Sep
PMID:Effect of ACTH on rabbit adrenal microsomal 17 alpha-hydroxylase activity, cytochrome P-450 and protein electrophoretic patterns. 610 Mar 44

Bromocriptine treatment in rats (3 mg/kg per day, 7 days) significantly reduced alpha-msh and aldosterone plasma levels 2 hrs after the final treatment in animals on low, normal and high sodium diets. Alpha-MSH dose response curves for corticosterone and 18-hydroxydeoxycorticosterone (18-OH-DOC) in subsequently incubated glomerulosa cells gave stimulation at lower concentrations of alpha-MSH (10(-10) moles per litre) than in cells from untreated animals (10(-9) moles per 1). Curves for aldosterone (ald) and 18-hydroxycorticosterone (18-OH-B) were also affected in cells from animals on a low sodium diet. Fasciculata-reticularis cell responses to ACTH were unaffected. Metoclopramide (4 mg/kg per day, 7 days) elevated plasma alpha-MSH, although ald was unaffected, but inhibited the glomerulosa cell response to alpha-MSH in vitro. Acute dopaminergic responses in plasma ald may be mediated through alpha-MSH in rats, but chronically alpha-MSH may down- regulate glomerulosa cell alpha-MSH receptors. It is unlikely that alpha-MSH mediates the adrenocortical response to sodium depletion.
Steroids 1982 Feb
PMID:Dopaminergic control of aldosterone: modulation of the response of rat adrenal zona glomerulosa cells to alpha-Msh by pretreatment with bromocriptine or metoclopramide. 628 Mar 45

The diurnal variations of the plasma concentrations of eleven steroid hormones and of corticotropin (ACTH) were studied in ten young healthy males. The plasma steroids progesterone, pregnenolone, deoxycorticosterone, 17-OH-progesterone, 17-OH-pregnenolone, deoxycortisol, 18-OH-deoxycorticosterone, corticosterone, aldosterone, cortisol and 18-OH-corticosterone, as well as plasma ACTH, were measured at 30-min intervals in the morning and in the evening and at 2-h intervals during the rest of the day. Steroids were extracted from 1 ml plasma, fractionated by high-pressure liquid chromatography (HPLC) and finally quantified by radioimmunoassay (RIA). Plasma concentrations of ACTH were radioimmunoassayed after extraction from 2 ml plasma. More or less pronounced circadian and episodic variations were apparent for plasma levels of all steroids studied, as well as of ACTH. According to related profiles of diurnal variations of plasma concentrations, three different categories of steroids were tentatively crystallized. Category 1 includes 17-OH-pregnenolone, deoxycortisol, corticosterone, 18-OH-deoxycorticosterone, deoxycorticosterone, cortisol and 18-OH-corticosterone, exhibiting a rhythm partly synchronous with that of the pituitary secretory activity of ACTH. Category 2, including progesterone, pregnenolone and 17-OH-progesterone, exhibited a time course of plasma concentrations assuming a regulation predominantly dictated by the testicular secretory activity. Lastly, aldosterone exerted a variation of plasma concentrations which was obviously regulated by the renin-angiotensin system under the present conditions.
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PMID:Diurnal and ultradian variations of plasma concentrations of eleven adrenal steroid hormones in human males. 628 2


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