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)

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

The changes in adrenocorticotropin (ACTH) release before, during and after sympathetic nerve degeneration following superior cervical ganglionectomy (SCGx) were examined in male rats. A 12-fold increase of circulating ACTH was found in both SCGx and sham-operated rats 6 h after surgery. In sham-operated rats, plasma ACTH decreased by about half 16-22 h after surgery, whereas in SCGx rats it remained at a high concentration from 16 to 54 h after surgery, attaining basal values by 120 h post-SCGx. In SCGx rats, MBH corticotropin-releasing hormone (CRH) content decreased significantly from 16 to 54 h after surgery, while in controls it remained unmodified. Significantly smaller arginine vasopressin (AVP) contents were found in MBH of SCGx rats as compared to sham-operated controls, 16-54 h after surgery. In rats exposed to ether or immobilization stress 22 h after SCGx, plasma ACTH levels were significantly higher than in controls; however, since unstressed ACTH levels were about twice as high in SCGx rats, the percent increase of ACTH was smaller in the SCGx group. A decreased response of plasma ACTH to ether or immobilization stress was found in rats 7 days after SCGx. In rats subjected to a simultaneous adrenalectomy (Adx) and SCGx or sham-SCGx, plasma ACTH levels increased to a similar extent in both groups. ACTH increase after Adx was accompanied by decreases in MBH CRH, and absence of significant changes in MBH AVP contents. Rats subjected to pinealectomy (Px) or sham-Px 1 week earlier and killed 22 h earlier exhibited similar responses in plasma ACTH and MBH CRH to SCGx regardless of pineal intactness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase in adrenocorticotropin release during wallerian degeneration of peripheral sympathetic neurons after superior cervical ganglionectomy of rats. 215 18

The effect of inescapable electric foot shock stress on vasopressin (VP) release was studied in conscious rats. In sham-operated animals, foot shock stress markedly increased plasma beta-endorphin-like immunoreactivity whereas plasma VP levels (RIA) remained unchanged. However, after selective ablation of the anterior lobe of the hypophysis, foot shock stress produced an 8-fold increase in plasma VP concentrations. Injection of hypertonic saline did not change plasma VP levels in adenohypophysectomized (Ahx) rats, while in sham-operated rats VP levels increased in response to this osmotic challenge. Neurointermediate lobes or medial basal hypothalami (MBH; containing the median eminence region) were superfused in vitro and stimulated electrically; as compared to sham operations, the evoked release of VP from the neurointermediate lobes was abolished, whereas that from the MBH was markedly (13-fold) enhanced when the tissues were taken from Ahx rats. The VP-like immunoreactivity released from the MBH of Ahx rats comigrated with synthetic arginine-VP on Sephadex G-15 column chromatography. Similarly, as found in Ahx rats, foot shock stress markedly raised plasma VP levels in totally hypophysectomized rats, whereas after selective ablation of the neurointermediate lobe of the hypophysis VP levels increased only slightly after stress. In conclusion, our data indicate that 1) foot shock stress induces the release of VP from some site other than the neurohypophysis, probably from the median eminence region, in Ahx rats; and 2) an increase in plasma osmolality is a powerful stimulus for the release of VP from the neurohypophysis but cannot release VP from the median eminence region. Thus, our results support the concept of a morphological and functional differentiation of the vasopressinergic neurosecretory system.
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PMID:Foot shock stress-induced release of vasopressin in adenohypophysectomized and hypophysectomized rats. 315 65

The effect of chronic administration of delta 9-tetrahydrocannabinol (delta 9-THC) on the endogenous opiate and catecholamine levels was investigated. Intact male rats were injected daily either with vehicle (50 microliters oil) or delta 9-THC in oil (3 mg delta 9-THC/kg body wt). The treatments were administered subcutaneously over a period of 25 days. All animals were decapitated after the last injection and trunk plasma was assayed for prolactin, beta-endorphin-like immunoreactivity (beta-end LI), norepinephrine (NE), epinephrine (E), dihydroxyphenyl acetic acid (DOPAC) and dopamine (DA). The preoptic area (POA) and medial basal hypothalamus were assayed for methionine enkephalin, beta-endorphin and catecholamines. Chronic delta 9-THC treatment resulted in an increase in POA and MBH methioine-enkephalin and beta-end LI as well as an increase in plasma beta-end LI. The POA, MBH and plasma NE and E levels were lower in these animals when compared with the controls. In the MBH, however, the delta 9-THC treated rats contained higher DA and DOPAC levels when compared with the controls. These results support our view that chronic delta 9-THC administration alters the activities of the endogenous opiate system as well as the catecholaminergic system and consequently impairs the endocrine functions.
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PMID:Effect of chronic administration of delta 9-tetrahydrocannabinol on the endogenous opioid peptide and catecholamine levels in the diencephalon and plasma of the rat. 609 37

We have previously shown that the hypothalamic concentration of immunoreactive alpha-melanotropin (alpha-MSHi) is markedly lower in the aging female rat than in the young rat. The current view is that alpha-MSH is derived from corticotropin (ACTH), and ACTH, in turn, is derived from a large molecular-weight precursor (pro-opiocortin); pro-opiocortin also serves as the precursor to beta- and gamma-lipotropin (LPH). To ascertain if the age-related reduction in the concentration of alpha-MSHi may be a result of a decline in the production of pro-opiocortin, we determined the content of immunoreactive ACTH (ACTHi), alpha-MSH (alpha-MSHi), gamma-LPH (gamma-LPHi), and protein, in 3 regions of the brain of young (4 months) and old (26-28 months) female rats: the medial basal hypothalamus (MBH, the region containing the perikarya of the ACTH/MSH/LPH neurons), the preoptic anterior hypothalamus (POA), and the thalamus (regions containing axons of these neurons). The concentration of ACTHi, alpha-MSHi (mol/mg protein), or gamma-LPHi (U/mg protein) in the MBH of old rats was 30-50% of that in the MBH of young rats. Moreover, the concentration of ACTHi, alpha-MSHi or gamma-LPHi in the POA and thalamus of old rats was also lower than that in the POA and thalamus of young rats. Based on these findings, we propose that aging causes a reduction in the production of pro-opiocortin in the brain of the female rat and that such a change may be related to the altered function of the brain of the aged.
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PMID:A reduction in the concentration of immunoreactive corticotropin, melanotropin and lipotropin in the brain of the aging rat. 632 11

We studied the effect of glucocorticoid pretreatment, mediobasal hypothalamus lesion (MBHL) and the interaction between clonidine and yohimbine in male Wistar rats to elucidate the sites and/or mechanisms of endocrine actions of alpha 2-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of alpha 2-antagonists yohimbine (5 mg/kg i.p.) and CH-38083 (1 mg/kg i.p.) on adrenocorticotropin (ACTH) secretion, while the action of these antagonists on prolactin (PRL) and beta-endorphin (beta E) remained unchanged. The central (i.c.v.) pretreatment of 5 micrograms/rat clonidine failed to antagonize the prolactin (PRL) and beta E releasing effect of yohimbine. However, it inhibited the yohimbine-induced ACTH secretion. MBHL resulted in a significant enhancement in basal plasma PRL and beta-endorphin (beta E) levels. But basal plasma ACTH levels have not been changed. Yohimbine failed to stimulate ACTH secretion in MBH-lesions rats, while PRL and beta E response to the yohimbine was maintained in these animals. This study confirms that the alpha 2-antagonists stimulate ACTH secretion by a corticosteroid-sensitive mechanism which is located centrally. In contrast, alpha 2-antagonists affect PRL and beta E secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.
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PMID:Adrenocorticotropin, prolactin and beta-endorphin stimulatory actions of alpha-2-adrenoceptor antagonists. 775 33

This article reviews data concerning the action of opioidergic and monoaminergic system on LHRH secretion. Generally, in anestrous ewes beta-endorphin and/or corticoliberin significantly change extracellular concentrations of monoamine metabolites in the MBH-ME, but in estrous ewes both beta-endorphin and CRF alters also dopamine, noradrenaline and serotonin levels. Responses of catecholaminergic and serotoninergic system in the MBH-ME to naloxone or CRF-antagonist depend, to a large degree, on the phase of reproduction. In anestrous ewes subjected to stressful stimuli an opiate receptor blocker, naloxone, and CRF-antagonist attenuate the stress - induced activity of catecholaminergic and serotoninergic system in the MBH-ME; in non-stressed animals they suppress only serotoninergic system activity in this structure. No clear explanation can be offered now for either differences in response of catecholaminergic and serotoninergic system in the MBH to beta-endorphin and CRF in various periods of reproduction or for differences in the responses of these systems to CRF antagonist and naloxone in non-stressed and stressed ewes. It has been suggested that the responses in monoaminergic system activity are highly dependent upon the physiological state of the animal and that beta-endorphin and corticoliberin may indirectly modulate LHRH and other hypothalamic hormone secretion by monoaminergic systems.
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PMID:Responses in the hypothalamic monoaminergic system activity in ewes to beta-endorphin, CRF and their antagonists. 891 9

Activation of the hypothalamus-pituitary-interrenal (HPI) axis is characteristic of stress responses, which may result from a variety of environmental challenges. To investigate whether the stress response, and in particular the HPI axis, in tilapia (Oreochromis mossambicus) is compromised by short-term exposure to PCB 126, fish of both sexes were fed diets containing PCB 126 (50 microg/kg fish . day) for 5 days. In the first approach, which was performed twice, fish were acutely stressed for periods varying between 1 and 30 min at the end of the exposure period; in the second approach fish were sampled at the end of the exposure period either at rest or after 2 h of stress (confinement). After 5 days, the body weights in all experiments were significantly lower in PCB-fed fish than in control fish. There were no changes in basal plasma glucose levels, plasma ion concentrations, or branchial, renal, and intestinal Na,K-ATPase activity following PCB exposure. In the first experimental approach, in which fish experienced acute sampling stress, plasma cortisol levels reached lower levels in PCB-fed fish than in controls. This suggests an impaired ability to acutely activate interrenal steroidogenesis in PCB-treated tilapia. Adrenocorticotropic hormone (ACTH)- and cAMP-stimulated in vitro cortisol release from superfused head kidneys was lower in tissues from tilapia exposed to PCB 126 than in tissues from control animals. This effect persisted after 24 h in vitro, which, together with the high PCB 126 concentrations measured in the head kidneys of PCB-fed fish, may indicate direct toxic effects on the interrenal cells. The second experimental approach demonstrated that basal plasma cortisol and ACTH levels were not influenced by PCB treatment, but that the basal ACTH content of the rostral pars distalis (RPD) of the pituitary gland of PCB-fed fish was lower than that of control fish. After 2 h confinement, plasma cortisol levels and ACTH content of the RPD rose to similar values in both groups, whereas plasma ACTH levels were higher in confined PCB-fed fish than in confined controls. PCB-fed fish showed a lower hyperglycemic response to confinement than control fish. Confinement resulted in similarly elevated renal and intestinal Na,K-ATPase activities in both PCB-fed and control fish; branchial enzyme activities were not affected. Since PCB did not affect Na,K-ATPase activities and plasma ion concentrations, it is concluded that the effects of PCB 126 on the HPI axis in tilapia are not secondary to ionoregulatory dysfunction.
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PMID:Interrenal stress responsiveness of tilapia (Oreochromis mossambicus) is impaired by dietary exposure to PCB 126. 940 23