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

The effect of corticotropin in vivo on total and specific protein synthesis in the adrenal was studied. Adrenal slices from control and corticotropin-treated animals were incubated with [14C]- and [3H]-leucine respectively, followed by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis of subcellular components. With this sensitive dual-labelling technique the following results were obtained. There was a general trophic effect on most adrenal proteins, but corticotropin produced a marked stimulation of a specific adrenal cytosolic protein. This protein has mol.wt. approx. 30 000 and pI 5.5. Corticotropin increased the incorporation of labelled leucine into proteins within 4 h, but no effect was observed before 2 h and after 16 h there was no further increase. These data suggest that this protein is not involved in the corticosteroidogenic action of corticotropin, but rather in the trophic action of this hormone.
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PMID:Effect of corticotropin treatment in vivo on the synthesis of a specific adrenal cytosolic protein. Characterization by dual-labelling technique and polyacrylamide-gel electrophoresis. 21 30

Adrenal responsiveness was evaluated by injecting 10 multiparous dairy cows with 200 IU adrenocorticotropin between -13 and -2 days prepartum (I) and postpartum between 24 and 40 h (II) and 21 and 24 days (III). Concentrations of glucocorticoids following injection were influenced by day of injection, temperature, and minimum percent relative humidity but not by breed, breed X injection day interaction, or age of cow. Likewise differences in regressions for adrenal response and mean response (ng/ml) for the three injections were nil. Mean concentrations at peak (45, 60, and 120 min postinjection samples) adjusted for preinjection concentrations also did not differ for the three periods of injection. Mean concentrations of glucocorticoids in plasma for daily samples between -13 and -2 days prepartum were 5.3 +/- .4 (n = 61), reached a peak of 14.8 +/- .3 ng/ml the day of calving, and remained high for 2 days postpartum. Estradiol increased through prepartum sampling from 23.3 to 339.6 +/- 94.1 pg/ml the day of calving, then declined abruptly. Progestins began to decline about -5 days prepartum from mean concentration of 4.09 +/- .62 (n = 25) and attained low concentrations (.30 +/- .06 ng/ml) 2 days postpartum. Although there was a surge of glucocorticoids at parturition, this was not associated with a modification in adrenal responsiveness or with prepartum concentrations of other steroid hormones of plasma. Adrenal potential in prepartum and postpartum dairy cows appears well maintained.
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PMID:Adrenal responsiveness in pre- and postpartum dairy cows. 21 98

In vitro adrenal accumulation of cyclic 3'5'-adenosine monophosphate (cyclic AMP) and release of corticosterone in response to adrenocorticotropic hormone (ACTH), cyclic AMP or theophylline was assessed in 60- and 340-day-old male rats. Adrenal tissue from mature animals secreted significantly smaller quantities of corticosterone in response to ACTH, theophylline or cyclic AMP. Additionally, mature tissue accumulated significantly less cyclic AMP after treatment with ACTH or a combination of ACTH and theophylline. The data suggest an age-related refractoriness of adrenal cortical tissue to ACTH which may in part be related to decreased availability of and/or sensitivity to cyclic AMP.
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PMID:Interaction of aging with in vitro adrenocortical responsiveness to ACTH and cyclic AMP. 22 Jan 72

We propose than an alarm mechanism is operative in animals, designed to regulate neuromuscular irritability by regulating [Ca2+]. Epinephrine or corticotropin (ACTH), injected intramuscularly into animals, causes a hypercitricemia, resulting in decreased [Ca2+]. This increases muscular excitability to facilitate escape. To avoid over reaction, [Cl-] is shifted into the plasma without a concomitant shift of Na+, thus generating an acidosis and an increase in ionization of Ca. Plasma pH, pCO2, total CO2, and [K+] decrease, and [Mg2+] increases. The acidosis, decrease in K+, and increase in [Mg2+] serve to counteract the effect of the decrease in [Ca2+], to protect against tetany. In the rabbit the hypercitricemia observed upon ACTH administration is accompained by a severe hypocalcemia and drop in blood pressure, resluting in tetanic convulsions. This seems to indicate calcitonin release, independent of the hypercitricemia. Thyroidectomized rabbits show only mild hypocalcemia when given ACTH, but develop a severe acidosis and typical grand mal epileptiform seizures. Administration of ACTH and then calcitonin to the goat, an animal resistant to the effects of ACTH alone, simulates the effect observed in the rabbit with respect to changes in blood components and blood pressure. Changes in the blood in the goat and rabbit resemble those in humans before an epileptic seizure. alpha-Melanotropin, containing a portion of the ACTH sequence, reacts in a manner similar to ACTH but more rapidly.
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PMID:Clinical biochemistry of epilepsy. II. Observations on two types of epileptiform convulsions induced in rabbits with corticotropin. 22 Nov 37

Tne Holstein heifers acclimated to either -2.7 or 19.1 C were used to determine glucocorticoid concentrations in plasma following injection of adrenocorticotropin (200 IU). Environmental treatments did not change glucocorticoids following adrenococorticotropin. Adrenocorticotropin injection elevated mean glucocorticoids to 41.6 ng/ml plasma at -2.7 C and 42.8 ng/ml at 19.1 C. Adrenal response to adrenocorticotropin in Holstein heifers was not altered by low environmental temperature.
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PMID:Adrenal response to adrenocorticotropin in Holstein heifers exposed to a cool environment. 23 14

A 64-yr-old female presented with severe osteoporosis and easy bruisability of over 2-yr duration. Biopsy of a neck mass revealed medullary carcinoma of the thyroid. Subsequently, lymphangitic pulmonary metastases were demonstrated which had been present radiographically for at least 4 yr. Basal serum calcitonin was markedly elevated and increased during calcium infusion. The diagnosis of ectopic ACTH syndrome was first entertained when hypokalemic alkalosis was observed during evaluation of her carcinoma. Elevated urinary 17-hydroxycorticosteroids, 17-ketosteroids, plasma cortisol, and immunoreactive plasma ACTH levels were documented. Adrenal steroidogenesis seemed to suppress on high dose dexamethasone. The primary tumor and its metastases contained high concentrations of immunoreactive ACTH and beta-melanocyte-stimulating hormone. Hepatic metastases contained extremely high concentrations of calcitonin. In contrast to the usual presentation of the ectopic ACTH syndrome as primarily hypokalemic alkalosis and glucose intolerance, patients with relatively benign and indolent ACTH-secreting tumors, such as certain cases of medullary carcinoma of the thyroid, may present with more typical signs and symptoms of Cushing's syndrome. The more pronounced cushingoid features in this latter group presumably reflects a more prolonged period of exposure to elevated glucocorticoid levels. Ten cases of ACTH-secreting medullary carcinoma of the thyroid from the literature are discussed. Extopic ACTH production by such tumors should be considered in the evaluation of patients with Cushing's syndrome or unexplained severe osteopenia.
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PMID:ACTH-secreting medullary carcinoma of the thyroid presenting a severe idiopathic osteoporosis and senile purpura: report of a case and review of the literature. 23 64

Spironolactone administration (50 mg/kg/day for 3 days) to make guinea pigs decreased cortisol production by adrenal slices in vitro. Adrenal microsomal and mitochondrial cytochrome P-450 levels were also decreased after treatment with spironolactone. The decline in adrenal cytochrome P-450 content was accompanied by decreases in microsomal 21-hydroxylase and mitochondrial cholesterol side-chain cleavage and 11beta-hydroxylase activities. Activities of other adrenal enzymes, such as delta4-hydrogenase and NADPH-cytochrome c reductase, were unaffected by spironolactone treatment. Cortisone administration to guinea pigs failed to mimic the effects of spironolactone on adrenal function, which indicates specificity of spironolactone action and excludes inhibition of adrenocorticotropin secretion as a mode of action. Addition of spironolactone to isolated adrenal mitochondria or microsomes produced type I spectral changes with spectral dissociation constants similar to those for endogenous steroid substrates. Spironolactone, in vitro, inhibited 11beta- but not 21-hydroxylase activity. The results indicate that spironolactone administration diminishes the activity of adrenal mitochondrial as well as microsomal cytochrome P-450-containing enzymes, resulting in a fall in corticosteroid output.
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PMID:Mechanism of action of spironolactone on adrenocortical function in guinea pigs. 97 70

A microperfusion system was developed to study detailed kinetics of adrenocorticotropic hormone (ACTH) secretion by dispersed rat anterior pituitary cells responding to various ACTH secretagogues. The system approaches hydrodynamics to square-wave stimuli and enables kinetic analysis of ACTH secretion with intervals as short as 5 sec. ACTH secretion initiated within 5 sec of exposure of the cells to corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT) or angiotensin II (A-II) and reached a maximum within 20-40 sec. CRF induced a plateau-shaped secretion of ACTH which remained constant as long as CRF was perifused. In contrast, the ACTH secretion responding to AVP, OT and A-II rose rapidly to a peak and fell to the baseline despite continued perifusion of these agents. There were two components of ACTH secretory response to AVP and OT. AVP had synergistic effect with CRF only if it was perifused simultaneously with CRF or immediately after CRF was stopped. The ACTH secretory response to A-II was greatly diminished when cells were exposed to AVP or OT before A-II perifusion. Prior exposure to A-II had no effect on the magnitude of the ACTH secretory response to either AVP or OT. Epinephrine, nor-epinephrine, gastrin-releasing peptide, atrial natriuretic factor and cholecystokinin stimulated no significant ACTH secretion in the microperfusion system, although some of them induced ACTH secretion by same cell preparation in static culture systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Physiological analyses of secretory kinetics of adrenocorticotropic hormone (ACTH) from anterior pituitary cells: development and application of a microperfusion system]. 131 80

Sixteen subjects (male, age: 26.3 +/- 3.5 years, weight: 75.1 +/- 6.5 kg, maximal oxygen uptake: 53.6 +/- 6.7 ml.min-1.kg-1) performed endurance exercises at 100% (exhaustive), and 85% (limited) of the individual anaerobic threshold [IAT; workload (100% IAT): 3.00 +/- 0.50 W.kg-1, duration of both exercises: 87 +/- 21 min]. Before (b), immediately (0 p), 60 min (60 p), 120 min (120 p) and 24 hours (24 hp) after exercise, leucocyte subpopulations (flow cytometry) as well as epinephrine, norepinephrine, cortisol, beta-endorphin and ACTH were determined. At 0 p, 60 p and 120 p, granulocytes were significantly higher at 100% IAT than at 85% IAT, lymphocytes and monocytes did not differ. At 60 p and 120 p, granulocytes had highest, lymphocytes lowest values. CD8(+)- and CD16(+)-lymphocytes showed greater changes than CD3(+)-, CD4(+)-, CD19(+)-lymphocytes and were significantly higher at 100% IAT than at 85% IAT (0 p). Epinephrine and norepinephrine were significantly higher at 100% IAT than at 85% IAT. Cortisol, ACTH and beta-endorphin increased at 100% IAT, but not at 85% IAT (0 p). Significant correlations were calculated for cortisol (0 p) versus granulocytes (60 p, 120 p) at 100% IAT. Epinephrine did not correlate to increases of lymphocytes or lymphocyte subpopulations. In conclusion, increases of granulocytes, CD16(+)- and CD8(+)-lymphocytes are dependent on the intensity of endurance exercises and precise definition of the individual workload is important. The increase of granulocytes after exercise is partly due to increased levels of cortisol. Increased cell numbers of lymphocytes, especially CD16(+)-cells, did not correlate to increased levels of catecholamines.
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PMID:Immunoregulatory hormones, circulating leucocyte and lymphocyte subpopulations before and after endurance exercise of different intensities. 132 59

The responses of the hypothalamic-pituitary-adrenal axis during chronic stress are characterized by normal or slightly elevated plasma ACTH, increased hypothalamic corticotropin-releasing hormone (CRH) and vasopressin secretion, decreased pituitary CRH receptors and hypersensitivity of the ACTH and glucocorticoid responses to a novel stress. To determine the role of CRH and vasopressin in the pituitary hyperresponsiveness to a superimposed stress, pituitary CRH receptors and plasma ACTH responses were measured in rats receiving minipump infusions of CRH or a combination of CRH and vasopressin (VP), 50 ng/min of each for 50 h. Rats were killed by decapitation with or without exposure to ether vapor for 5 min or immobilization for 15 or 30 min, and blood was collected for ACTH and corticosterone determinations. The pituitary CRH receptor concentration measured by binding 125I-Tyr-oCRH, was reduced by 45 and 80% in CRH- and CRH-plus-VP-infused rats, respectively, with no changes in receptor affinity. Acute stress by ether exposure or immobilization had no effect on pituitary CRH receptors. Adrenal weight was significantly increased, and thymus weight decreased in CRH-infused animals, indicating activation of the pituitary adrenal axis. However, in contrast to the responses following chronic stress, the increases in plasma ACTH in response to an injection of 10 micrograms/kg CRH or acute stress were significantly lower in CRH- and CRH-plus-VP-infused rats. Furthermore the content and release of ACTH from quartered pituitaries were also decreased in chronically treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Desensitization of the hypothalamic-pituitary-adrenal axis following prolonged administration of corticotropin-releasing hormone or vasopressin. 133 16


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