Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous experiments demonstrated that increases in ovine fetal plasma cortisol concentration to maximal stress levels suppressed fetal plasma renin activity and completely inhibited fetal adrenocorticotropin (ACTH) responses to subsequent stress. This study was designed to quantitate the suppressive action of cortisol on both ACTH and renin. Fetal sheep between 117 and 131 days gestation were surgically prepared with chronically implanted catheters. At least 4 days after surgery, vehicle or cortisol (0.25, 0.5, 1, 2, or 3 micrograms/min) were infused for 5 h. One hour after the end of the vehicle or cortisol infusion, fetal ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside. Cortisol infusions suppressed basal plasma renin activity (caused by suppression of plasma renin concentration) to degrees that were related to the increases in fetal plasma cortisol concentration. After cortisol infusions, renin responses to hypotension were apparently suppressed to degrees not obviously related to the rate of cortisol infusion. Fetal plasma ACTH responses to hypotension were completely suppressed by increases in total and unbound fetal plasma cortisol concentration 1.6 and 1.7 ng/ml, respectively. These results demonstrate a high sensitivity of the fetal hypothalamopituitary unit and renin-angiotensin system to cortisol.
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PMID:Sensitivity of cortisol-induced inhibition of ACTH and renin in fetal sheep. 301 Jul 46

A circannual analysis was made of serum cortisol, luteinizing hormone (LH), and testosterone concentrations in the male clouded leopard (Neofelis nebulosa). Group I males (n = 4), maintained in a standardized environment, were bled serially during a regimented anesthesia/electroejaculation episode occurring monthly (beginning in January, ending in December). Additional sampling intervals were conducted under anesthesia only (control, n = 8), anesthesia plus a single adrenocorticotropin hormone challenge (ACTH, Cortrosyn, n = 4), or anesthesia plus a single 25 micrograms injection of gonadotropin-releasing hormone (GnRH, Gonadorelin, n = 4). Group II males (n = 6) from various zoological collections were sampled serially under the same semen collection conditions on one random occasion within the year. Serum cortisol levels were 2 times greater than values measured in comparable studies involving other felid species. Cortisol concentrations were similar during electroejaculation and control (anesthesia only) episodes, and mean levels did not rise as a result of semen collection. Adrenocorticotropin caused an immediate rise in cortisol to levels at least 1.5 times greater than electroejaculated or control counterparts. Mean concentrations of basal cortisol in individual males gradually increased as the year progressed, possibly as a consequence of repeated psychogenic stress. Between seasons, there were no differences in mean LH; however, testosterone levels were greater (p less than 0.05) in the winter compared to all other seasons. There were no differences (p greater than 0.05) between individual males in secretory patterns or mean concentrations of cortisol, LH, or testosterone. Within males, distinct temporal fluctuations were observed in both LH and testosterone during the approximately 80-min sampling interval. Neither LH nor testosterone profiles appeared affected by cortisol patterns during electroejaculation or after an ACTH challenge. A bolus of GnRH induced a marked rise in serum LH and testosterone within 15 and 30 min respectively, indicating that these two hormones were coupled. Both LH and testosterone profiles in Group II males mimicked those in Group I; concentrations of cortisol in Group II males immobilized on one occasion were similar to those of Group I animals sampled from January-May but appeared to be less than values measured from June-December. These data demonstrate that the clouded leopard, compared to other felids, produces markedly elevated concentrations of cortisol, which are likely related to an aggressive behavioral temperament.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reproductive physiology of the clouded leopard: II. A circannual analysis of adrenal-pituitary-testicular relationships during electroejaculation or after an adrenocorticotropin hormone challenge. 301 73

Dexamethasone-suppressible hyperaldosteronism is a rare familial syndrome in which hypokalemia, suppression of plasma renin concentration, and elevated aldosterone secretion are corrected by treatment with glucocorticoids. Regulation of adrenocortical function and body electrolytes was studied in two affected brothers. Both were hypertensive (210/128 and 160/106 mm Hg) with hypokalemia (3.3 and 3.5 mM) and low plasma renin concentrations. Aldosterone was elevated intermittently with levels as high as 45 ng/dl (normal range, 4-16 ng/dl). Cortisol concentrations were normal but were correlated with aldosterone levels (r = 0.9 and 0.7). Concentrations of 11-deoxycorticosterone (19 and 21 ng/dl; normal range, 4-16 ng/dl) and 18-hydroxycortisol (1000 and 950 ng/dl; normal range, 34-150 ng/dl) were elevated, and diurnal changes in both were the same as those seen with aldosterone. Infusion of adrenocorticotropic hormone (ACTH) caused exaggerated increases of aldosterone, 11-deoxycorticosterone, and 18-hydroxycortisol; cortisol response was normal. A 4-week trial of dexamethasone normalized blood pressure and caused a natriuresis, a fall in aldosterone, and a rise in plasma renin. Administration of ACTH after dexamethasone treatment again caused exaggerated increases of aldosterone. Aldosterone did not respond to angiotensin II before dexamethasone therapy (r = 0.01), but it showed a normal response after therapy (r = 0.8, p less than 0.01). Neither administration of dopamine (1 microgram/kg/min) nor long-term therapy with bromocriptine (2.5 mg t.i.d. for 4 weeks) affected aldosterone biosynthesis. Thus, loss of dopaminergic inhibition of mineralocorticoid biosynthesis does not account for hyperaldosteronism in this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia? 301 96

Tissues from 12 human corticotropin-secreting adenomas, obtained during surgery for Cushing's disease (CD, ten cases) or Nelson's Syndrome (NS, two cases), were exclusively mechanically dispersed. Single cells and cell aggregates were plated on extracellular matrix derived from bovine corneal endothelia. Functional responses to physiological stimuli were analyzed by measuring human beta-endorphin (beta h-EP) immunoreactivity (IR) by radioimmunoassay in the culture medium. All adenomas responded with stimulated secretory activity to arginine vasopressin (AVP), corticotropin-releasing factor (CRF), or both. Cortisol higher than 10(-8) M suppressed basal secretion and CRF- or AVP-stimulated beta h-EP-IR secretion. There was no consistent difference in response of the cells when cultured in medium containing 10% fetal calf serum (FCS) or in serum-free conditions. A change of cells from serum to serum-free conditions usually resulted in 10%-50% reduction in the basal secretion level that remained stable for at least 2 weeks and, in one case (NS), 10 weeks. In cells maintained in medium supplemented with 5% serum obtained from the respective patients 40 min after adenoma removal, basal secretion was suppressed to 60% of the baseline level in a 10% FCS control. Long-term incubation with CRF (10(-9) M) showed sustained stimulation of hormone secretion. No remarkable cell proliferation was observed under basal conditions or during long-term, low-dose incubation with cholera toxin (10(-12) M) in two cases (CD), or CRF (10(-9) M) in two cases (NS, CD). Parallel beta-EP-IR and adrenocorticotropin secretion was verified in selected cases.
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PMID:Long-term culture of human corticotropin-secreting adenomas on extracellular matrix and evaluation of serum-free conditions. Secretory aspects. 302 31

Expression of proopiomelanocortin (POMC) was studied in a male patient with Cushing's syndrome and ectopic production of ACTH by a pancreatic carcinoma. Plasma ACTH levels (greater than 200 pg/ml) were elevated, and elevated serum cortisol and urinary free cortisol were partially suppressed to 25% of basal levels by high-dose dexamethasone. Petrosal and jugular vein sampling did not yield a gradient of ACTH. Immunohistochemical staining of tumor tissue removed at pancreatectomy was positive for ACTH and beta endorphin, and negative for corticotropin-releasing factor (CRF). Tumor cells cultured in vitro secreted ACTH and beta-endorphin, which comigrated with their respective radiolabeled standards on gel chromatography. Hydrocortisone suppressed in vitro ACTH secretion and CRF (100 nM) stimulated ACTH by 50% during 72 hours of incubation. Agarose gel electrophoresis of poly-(A) mRNA extracts of tumor tissue followed by hybridization with 32P-cDNA for POMC revealed 2 distinct RNA species. The major RNA species (about 1.0 kb) was smaller than authentic pituitary POMC mRNA (about 1.1 kb); a larger precursor band also was visualized, suggesting either processing or degradation of tumor-POMC mRNA. Cytoplasmic dot blot hybridization of tumor mRNA with POMC cDNA yielded a positive signal with increasing amounts of RNA blotted. Immunohistochemistry and radioimmunoassay (RIA) of ACTH, in vitro regulation of ACTH secretion, and expression of POMC mRNA species by this tumor document expression of the human POMC gene by an islet carcinoma associated with Cushing's syndrome.
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PMID:Cushing's syndrome due to ectopic proopiomelanocortin gene expression by islet cell carcinoma of the pancreas. 302 8

Some of the interrelations of neuroendocrine changes associated with hypovolemia were investigated in a model simulating an arterial hemorrhage. beta-Endorphin, adrenocorticotropin hormone (ACTH), and cortisol levels were measured by radioimmunoassay before, during, and after controlled bleeding of conscious splenectomized pigs. All animals showed significant (P less than 0.05) increases in the three neuroendocrine substances during hemorrhage. beta-Endorphin values initially were 55 +/- 7 pg/ml (+/- SE) and rose to a peak of 386 +/- 44 pg/ml at the nadir of blood pressure (mean arterial pressure = 47.5 mmHg). ACTH showed a similar pattern, increasing from 49 +/- 10 to a peak of 518 +/- 56 pg/ml. Cortisol values reached their peak of 18.2 +/- 2.5 micrograms % during the recovery phase. beta-Endorphin values displayed a close inverse correlation to blood pressure during hemorrhage, but returned to basal levels more rapidly than blood pressure during the recovery period. Plasma ACTH levels rose significantly more slowly than beta-endorphin as the hemorrhage progressed. An equimolar ratio of ACTH and beta-endorphin returned only as levels declined following the hemorrhagic insult. In awake pigs therefore an arterial hemorrhage is accompanied by endorphin release proportional to the decrement in blood pressure, a somewhat retarded buildup of ACTH, and a still later cortisol peak during recovery.
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PMID:Beta-endorphin, ACTH, and cortisol response to hemorrhage in conscious pigs. 303 83

beta-Endorphin (beta-EP), beta-lipotropin (beta-LPH) and cortisol plasma levels were measured during labor in 18 pregnant women. In 7 cases labor progressed spontaneously and in 11 cases oxytocin (5 mIU/min) was administered to stimulate uterine contractions. In control and oxytocin-treated subjects hourly blood samples were taken until delivery. In spontaneous labor all three hormones showed a progressive and significant increase until parturition. In oxytocin-treated patients, however, both beta-EP and beta-LPH remained constant until parturition. Cortisol levels in oxytocin-treated patients presented a significant increase but reached values significantly lower than in control patients. These results indicate that women with uterine hypocontractility during labor requiring oxytocin showed no rise in their plasma beta-EP and beta-LPH and a blunted cortisol rise during oxytocin administration.
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PMID:Lack of beta-endorphin plasma level rise in oxytocin-induced labor. 316 Jun 39

The effects of chronic glucocorticoid treatment on sympathoadrenomedullary function were assessed in conscious unrestrained Wistar-Kyoto rats. Cortisol (25 mg/kg.day), administered for 7 days using a sc reservoir pump, suppressed activity of the hypothalamo-pituitary-adrenocortical axis, as indicated by markedly decreased levels of corticotropin (ACTH) and corticosterone and decreased adrenal weight. Cortisol also decreased body weight and increased blood pressure to hypertensive levels without affecting plasma sodium or potassium. Basal levels of plasma epinephrine were markedly decreased, indicating suppression of adrenomedullary secretion. Plasma norepinephrine levels also were decreased, but to a smaller extent than epinephrine, and levels of dihydroxyphenylglycol, an intraneuronal metabolite of norepinephrine, were unaffected. Plasma catecholamine responses to nitroprusside-induced hypotension were not altered by cortisol. The results suggest that chronic cortisol treatment suppresses basal hypothalamo-pituitary-adrenocortical and basal adrenomedullary activity in conscious unrestrained rats without impairing reflexive activation of the sympathoadrenomedullary system.
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PMID:Sympathoadrenomedullary inhibition by chronic glucocorticoid treatment in conscious rats. 316 35

The effect of hydrocortisone (hydrocortisone sodium succinate) on bovine lymphocyte blastogenesis in response to Staphylococcus aureus antigens and phytohemagglutinin was measured in vitro. Lymphocytes isolated from the blood of cows were treated for 6 to 8 days with physiologic hydrocortisone concentrations known to be inducible by environmental stress (10 ng/ml), acute clinical mastitis (25 ng/ml), or adrenocorticotropin treatment (45 ng/ml). All 3 concentrations of hydrocortisone caused a depression (P less than 0.01) in lymphocyte blastogenesis in response to phytohemagglutinin and S aureus antigen extract. Hydrocortisone concentrations as low as 10 pg/ml caused a depression in the lymphocyte blastogenic response to phytohemagglutinin. Marked variation existed among cows in the normal response of their nontreated lymphocytes and in the degree of depression of lymphocyte function after the in vitro treatment with hydrocortisone. Macrophage depletion experiments showed that the suppressive effect of hydrocortisone was not mediated by induction of suppressor macrophages. The data suggest that T-cell function was impaired directly by hydrocortisone treatment.
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PMID:In vitro depression of bovine lymphocyte function by treatment of cultured bovine lymphocytes with physiologic concentrations of hydrocortisone. 340 Sep 21

In order to verify whether fetal and maternal adrenal gland suppression induces effects on fetal behaviour, triamcinolone was administered to five healthy pregnant women at 35 weeks of gestation. Five patients of the same gestational age were used as control. Fetal heart rate (FHR) and fetal movements were recorded continuously over 2-h interval by means of cardiotocography. After 3 weeks (38 weeks of gestation) the recordings were repeated without drug administration. Cortisol, adrenocorticotropin hormone, 17 beta-estradiol and unconjugated estriol were measured at the same time every 2 h in maternal peripheral plasma. At 35 weeks we found a loss of circadian rhythms of the hormones investigated and modifications of ultradian and circadian patterns of FHR in the treated group with respect to the control. No differences in hormonal and biophysical parameters were found between the two groups after the end of treatment (38 weeks). These data suggest that the inhibition of fetal and maternal adrenal glands could cause modifications of FHR patterns.
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PMID:Modifications of ultradian and circadian rhythms of fetal heart rate after fetal-maternal adrenal gland suppression: a double blind study. 380 12


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