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

The present study was undertaken to determine the structure-activity relationships of ACTH analogs on corticosteroid production by frog adrenal gland. Rana ridibunda interrenal dice were perifused with amphibian culture medium for 10 hr. Corticosterone and aldosterone concentrations were measured in the effluent perifusate using sensitive and specific radioimmunoassay methods. Perifusion of interrenal fragments with increasing concentrations of synthetic human ACTH 1-39 (ranging from 6.25 X 10(-11) to 10(-9) M) led to a linear log-dose increase in both corticosterone and aldosterone secretion. Thus, this model made it possible to compare the steroidogenic potency of several ACTH analogs. Synthetic alpha-MSH and its des-N alpha-acetyl derivative were found to be approximately equipotent, and 5 X 10(3) times less active than authentic ACTH. The short-chain analog ACTH 1-10 was 2 X 10(4) times less potent than ACTH whereas ACTH 4-10 was totally inactive. A fragment of the N-terminal region of the proopiomelanocortin molecule, gamma 3-MSH, caused a dose-related stimulation of steroid secretion. However, in contrast to what has been observed in the rat, gamma 3-MSH did not potentiate the corticotropic action of ACTH on frog interrenal gland. Since processing of proopiomelanocortin in frog intermediate lobe generates high amounts of alpha-MSH and des-N alpha-acetyl alpha-MSH, these results suggest that in amphibians, several peptides other than ACTH may be involved in the control of corticosteroidogenesis.
 ...
PMID:In vitro study of frog (Rana ridibunda Pallas) interrenal function by use of a simplified perifusion system. VIII. Structure-activity relationship of synthetic ACTH fragments and gamma-MSH. 300 66

The effect of beta-endorphin (beta-END) and the role of the adrenal and thyroid glands on body temperature were examined in male rats in a controlled environment room at 24.5 +/- 0.1 degrees C. Relative humidity of 50 +/- 0.3% and a 12L:12D photoperiod (L = 0900 to 2100 hr) were maintained. Rectal temperature (Tr) was measured using thermistors. Corticosterone and thyroid hormones were determined by radioimmunoassay. Intracerebroventricular (IVT) administration of varying doses (0.05 to 50.0 micrograms) of beta-END resulted in a hyperthermia that began 30 min post-IVT injection and continued for an additional hour. Intravenous injections of the same doses of beta-END resulted in little or no Tr response. The beta-END-induced hyperthermia was antagonized by intraperitoneal injection of naloxone. Pretreatment with propranolol, phenotolamine, or both drugs in combination did not block the hyperthermia caused by beta-END. Adrenalectomized or hypophysectomized rats receiving IVT injections of beta-END did not consistently display an increased Tr. beta-Endorphin administration had no detectable effect on serum corticosterone or thyroxine but serum triiodothyronine was decreased. These data suggest the acute hyperthermic action of beta-END is mediated centrally through opiate receptors and does not involve adrenergic receptors.
 ...
PMID:Adrenal and thyroid interactions of beta-endorphin-induced body temperature responses of rats at 24.5 degrees C. 315 82

We examined the effect of rotation-induced stress on (1) growth of lymphosarcoma tumors; (2) interleukin-2 (IL-2) production; (3) T cell subset distribution; and (4) cytotoxic T cell (CTL) function. In addition, we examined the levels of corticosterone and beta-endorphin as possible mediators of stress-induced immune alterations. Rotation stress induced progressive lymphosarcoma growth, while unstressed mice showed tumor regression after 2 weeks of growth. IL-2 production and CTL activity in stressed animals were significantly lower than controls during the first 2 weeks after initiation of stress. Spleen lymphocytes from stressed and control mice bearing the L3T4 antigen (helper/inducer T cell marker) remained unchanged, while in peripheral blood such cells decreased in stressed but not control animals. This latter pattern was also observed in Lyt 2 positive (suppressor/cytotoxic) cells of both spleen and peripheral blood. Corticosterone levels were elevated for an extended period following initiation of stress, while beta-endorphin levels remained similar to those of the controls. Although these data do not directly establish a causal link between immunoinhibition and tumor growth, they clearly demonstrate that stress inhibits a number of cell-mediated immune functions that may be relevant in this regard.
 ...
PMID:Stress-induced decline in immune responsiveness in C3H/HeJ mice: relation to endocrine alterations and tumor growth. 326 57

Ten-week-old female obese and lean Zucker rats were given access to three separate macronutrient sources (casein, starch, and lard) for 7 days. They were then either adrenalectomized (ADX) or given a sham operation. Rats were assigned to one of three groups and given a daily injection of either 0, 2, or 10 mg of corticosterone. They continued to select a diet for another 17 days, after which they were killed, and their blood was assayed for corticosterone, adrenocorticotropin hormone (ACTH), insulin, glucose, and triglyceride. Retroperitoneal and parametrial fat depots were excised and sampled for lipoprotein lipase activity, fat cell size, and number. Body composition was also determined. Selection patterns of lean and obese rats were markedly affected by both ADX and corticosterone replacement. All three groups of sham-operated obese rats ate significantly more fat than did sham-operated lean rats. Adrenalectomy significantly reduced fat intakes in both obese and lean rats. Corticosterone therapy restored fat appetites of lean and obese rats in a dose-dependent fashion. In comparison to ADX lean rats, ADX obese rats reduced their normally elevated levels of blood glucose, plasma triglycerides, and insulin to within normal limits. Similarly, adipose cellularity of the ADX obese rats was reduced to that of sham-operated lean rats. Carcass fat was significantly reduced after adrenalectomy. Corticosterone therapy prevented the reduction in a dose-dependent way.
 ...
PMID:Some metabolic and behavioral effects of adrenalectomy on obese Zucker rats. 377 20

Immunologically and biologically active ACTH, as well as biologically active alpha-MSH were secreted by monolayer cultures of rat pituitary intermediate lobe cells. The release of the immunoreactive ACTH and the bioactive alpha-MSH was inhibited by dopamine and by the dopamine agonist bromocriptine. The inhibition is probably mediated by specific dopaminergic receptors, since simultaneously added haloperidol prevented the dopamine induced hormone release inhibition. Pro-Leu-Gly-NH2, a potent inhibitor of the alpha-MSH secretion, had no effect on the release of ACTH. Synthetic ovine CRF stimulated the release of both immunoreactive ACTH and bioactive alpha-MSH in dose-dependent fashion. Corticosterone was without effect on hormone release in the cultures derived from both adrenalectomized and sham-operated animals.
 ...
PMID:Responsiveness of intermediate lobe cells to neural mediators in culture. 609 87

A 41-residue peptide purified as a corticotropin-releasing factor/beta-endorphin-releasing factor (CRF) in vitro was tested for its ability to stimulate the secretion of ACTH, beta-endorphin, and corticosterone in three animal groups: 1) unanesthesized rats bearing indwelling venous cannulae, 2) rats pretreated with chloropromazine plus morphine sulfate plus pentobarbital (CPZ-MS-Nb, and 3) rats with hypothalamic deafferentiations in the frontal and lateral retrochiasmatic areas. In all three bioassays iv administration of 0.1-10 micrograms CRF elicited a dose-related increase in plasma ACTH and beta-endorphin values over a 5- to 15-min period. Corticosterone secretion was also elevated but responded maximally with all doses of CRF tested. Pretreatment of CPZ-MS-Nb animals with 20 micrograms dexamethasone 4 h before assay abolished the CRF-induced hormone secretion. These data suggest that CRF may play a physiological role in the regulation of the hypothalamic-pituitary-adrenal axis.
 ...
PMID:In vivo corticotropin-releasing factor-induced secretion of adrenocorticotropin, beta-endorphin, and corticosterone. 627 23

The role of end-product glucocorticoids in the regulation of corticosteroidogenesis in isolated adrenocortical cells was investigated. Trypsin-isolated cells from male rat adrenal glands were incubated with or without corticotropin (ACTH) and with or without corticosterone. Endogenous corticosterone production was determined by radioimmunoassay at the end of incubation. Cessation of ACTH-induced corticosterone production was apparent after 2-4 h of incubation. The suppression occurred later with lower cell concentrations. Corticosterone production was partially restored after washing the suppressed cells. Supernatant fluid from suppressed cell suspensions also suppressed steroidogenesis of a fresh population of cells. However, the suppressing property of the supernatant fluid was abolished after the removal of corticosterone by charcoal-dextran treatment, suggesting that corticosterone or other steroids caused the suppression. Exogenous corticosterone induced suppression over a wide range of ACTH concentrations, but did not change the half-maximal steroidogenic concentration of ACTH, indicating that the suppression does not change the sensitivity of the cells to ACTH. Suppression occurred within 30-60 min after corticosterone had been added to the incubation medium either at the start of incubation or while steroidogenesis was in progress. Suppression varied directly with the concentration of exogenous corticosterone. These data indicate that glucocorticoids can directly and acutely suppress corticosteroidogenesis and thus control adrenocortical function in concert with other regulators such as ACTH and Ca2+.
 ...
PMID:Glucocorticoid control of steroidogenesis in isolated rat adrenocortical cells. 630 94

The responses of rat adrenal zona glomerulosa cells to stimulation by alpha-MSH and ACTH and related peptides have been studied. The major findings were that: (1) alpha-MSH stimulated corticosterone production in glomerulosa cells from from normal animals at concentrations of about 10(-10) mol/l, but other steroids, including aldosterone, were not significantly stimulated until levels of 10(-7) mol/l were used. Peptide structure-function relationships showed that in the adrenal cortex, in contrast with other systems, ACTH 4-10 had no effect and did not block the response of glomerulosa cells to alpha-MSH, bisacetyl Ser 1-alpha-MSH, (nor-valine-12)-alpha-MSH, and ACTH 1-13 amide were equipotent with alpha-MSH, while alpha-MSH 1-10 had activity but was considerably less potent. alpha-MSH 6-13, 7-13, 8-13 and lys-11-acetyl-alpha-MSH were all inactive. N-formyl-N-epsilon-benzyloxycarbonyl alpha-MSH stimulated only at 10(-6) mol/l. (2) Normalised alpha-MSH dose-response curves for aldosterone production in glomerulosa cells from normal rats, and corticosterone in inner zone cells were coincident. In glomerulosa cells, prior sodium depletion shifts the dose-response curve for aldosterone to the left, indicating a more sensitive response, and for corticosterone to the right. Bromocriptine treatment (which depresses the level of alpha-MSH in circulating plasma) and metoclopramide (which enhances it) respectively increased and decreased the sensitivity of the response of corticosterone to alpha-MSH in subsequently incubated glomerulosa cells, but had no effect on aldosterone. (3) In contrast, normalised ACTH stimulated dose-response curves for glomerulosa corticosterone and aldosterone, and for fasciculata corticosterone production were all coincident, and were unaffected by sodium depletion, or by metoclopramide or bromocriptine pretreatment. (4) Cyclic-AMP production by glomerulosa cells was stimulated by alpha-MSH only at levels of in excess of 10(-5) mol/l, five orders of magnitude greater than required to produce significant corticosterone stimulation. Under cyclic-AMP stimulation, the normalised responses of glomerulosa corticosterone and aldosterone, and of inner zone corticosterone were all coincident. The data suggest that alpha-MSH at low concentrations (less than 10(-7) mol/l) interacts with a glomerulosa cell receptor which is distinct from the ACTH receptor but interacts with the ACTH receptor at concentrations greater than 10(-'5) mol/l. Corticosterone production is stimulated by alpha-MSH in cells from normal animals at concentrations within the normal range for circulating plasma (approximately 3 X 10(-10) mol/l), while aldosterone is stimulated by similar concentrations of alpha-MSH in cells from sodium depleted animals. The effects of sodium depletion are not modulated through changes in plasma alpha-MSH levels. At low concentrations alpha-MSH stimulation of glomerulosa cells is unlikely to be modulated by cyclic-AMP as second messenger.
 ...
PMID:alpha-MSH and zona glomerulosa function in the rat. 631 Feb 42

The finding that some opioid-mediated forms of stress-induced analgesia are antagonized by hypophysectomy and dexamethasone has led to the suggestion that beta-endorphin, released from the pituitary, may mediate these analgesic reactions. "Long-term analgesia" (an opioid-mediated form of stress-induced analgesia), which is blocked by dexamethasone and hypophysectomy, was also blocked by adrenalectomy and reinstated with corticosterone therapy. Corticosterone is proposed to play a permissive role in long-term analgesia and to be a critical hormone mediating this phenomenon.
 ...
PMID:Corticosterone: a critical factor in an opioid form of stress-induced analgesia. 706 62

Arginine-vasopressin (AVP) markedly increased basal aldosterone (ALDO) secretion by dispersed zona-glomerulosa (ZG) cells, and its effect was selectively reversed by V1-receptor antagonists (AVP-A1). Corticosterone (B) production by dispersed zona fasciculata (ZF) cells was not affected. The bolus intraperitoneal (i.p.) administration of AVP acutely raised the plasma concentrations of both ALDO and B in normal rats, but only that of ALDO in bilaterally adrenalectomized animals bearing regenerated adrenocortical autotransplants, which are deprived of medullary chromaffin cells. Accordingly, AVP raised ALDO and B secretions by adrenal slices (including both cortical and medullary tissues), and only ALDO production by autotransplant quarters. The B response of adrenal slices to AVP was blocked by alpha-helical-CRH and corticotropin-inhibiting peptide (two competitive inhibitors of CRH and ACTH, respectively), but not by 1-alprenolol (a beta-adrenoreceptor antagonist); ALDO response was not affected by any of these antagonists. A 7-day i.p. infusion with AVP increased the volume of ZG cells and ZG-like cells of autotransplants, as well as their basal and maximally angiotensin-II-stimulated ALDO secretory capacity; it also raised the volume, and basal and maximally ACTH-stimulated B secretory capacity of ZF cells, but it did not affect ZF-like cells of autotransplants. The simultaneous administration of AVP-A1 annulled all these effects of AVP. When infused alone, AVP-A1 caused a marked atrophy of ZG cells, coupled with a net drop in their steroidogenic capacity; however, AVP-A1 infusion did not change the morphology and function of either ZF cells or ZG-like and ZF-like cells of autotransplants. Taken together,, our findings allow us to draw the following conclusions: (i) AVP plays an important physiological role in the maintenance and stimulation of ZG growth and mineralocorticoid secretory activity in rats, the source of endogenous AVP exerting adrenoglomerulotropic action probably being adrenal chromaffin cells; and (ii) AVP indirectly stimulates the growth and glucocorticoid secretory activity of rat ZF cells, by activating intramedullary CRH/ACTH system; however, the physiological relevance of this effect of AVP appears to be doubtful.
 ...
PMID:In-vitro and in-vivo studies of the effects of arginine-vasopressin on the secretion and growth of rat adrenal cortex. 759 33


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>