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)

Because hypothalamic and extrahypothalamic levels of thyrotropin-releasing hormone immunoreactivity (TRH-IR) undergo profound changes during the prenatal and early postnatal period in rats, similar effects with advanced aging were anticipated. For this reason we measured hypothalamic and reproductive tissue levels of TRH-IR, hypothalamic levels of somatostatin (SRIF), and beta-endorphin (EP), serum levels of prolactin (Prl), growth hormone (GH), thyrotropin (TSH), and thyroxine (T4) in young, sexually mature and 24-28 month-old male Long-Evans and Sprague-Dawley rats. Hypothalamic and prostatic levels of TRH-IR were consistently reduced as were the levels of T4 in old rats compared to young controls. Aging did not change the ratio of TRH to the major TRH-like peptide in prostates, as determined by high pressure liquid chromatography (HPLC) or the levels of hypothalamic SRIF and EP. All of the hypothalamic TRH-IR in both old and young male rats consisted of TRH by HPLC. Falling hypothalamic TRH levels and TRH secretory capacity may play a role in the blunted TSH response to cold stress in old rats.
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PMID:Thyrotropin-releasing hormone levels decrease in hypothalamus of aging rats. 615 Nov 24

1 Morphine and related synthetic surrogates as well as beta-endorphin and methionine enkephalin caused a contractile response of the longitudinal musculature of the terminal colon of Long Evans rats.2 The muscular contraction caused by the narcotic analgesics exhibited stereospecificity, with levorphanol being about 50 times more potent than dextrorphan and (-)-methadone 4 times more potent than (+)-methadone. In addition, the rank order in potency of a homologous series of N-alkyl substituted norketobemidones demonstrated that the activity of these compounds in eliciting contractile responses corresponded to that for analgesic efficacy in the rat and also correlated to the ability of these derivatives to inhibit the muscular twitch evoked by electrical stimulation of the guinea-pig ileum.3 Naloxone blocked the contractile response of the opiates following competitive kinetics; the naloxone pA(2) values for morphine, etorphine, levorphanol and methadone were very close, in spite of the marked differences in potency of these agents.4 The contractile effect of morphine on the rat colon was abolished by incubation of the tissues with tetrodotoxin 2.0 x 10(-7) M or by decreasing the external Ca(2+) level 100 fold. Increasing the external Ca(2+) concentration caused an apparent non-competitive antagonism of the response to morphine.5 Pretreatment of the tissues with hexamethonium 8.3 x 10(-5) M caused a modest antagonism of the morphine effect while atropine 5.8 x 10(-7) M did not significantly modify the morphine contractile effect. In contrast, methysergide 10(-5) M caused a 10 fold increase in the morphine EC(50).6 Colons from rats rendered tolerant-dependent on morphine were markedly less sensitive to the contractile effects of morphine than those from placebo-treated controls. Tolerance to morphine was also accompanied by an increased sensitivity to the contractile effects of 5-hydroxytryptamine (5-HT).7 A marked increase in the spontaneous muscular activity of segments of the terminal colon of rats chronically treated with morphine was found to occur upon removal of the residual morphine in the tissues by repetitive washings. The spontaneous activity was arrested by applications of morphine, suggesting that physical dependence can be demonstrated in vitro in this particular preparation.8 It is concluded that the opiate-induced contractile response is mediated via stereospecific, naloxone-sensitive, opiate receptors and that the muscular response involves the activation of a 5-HT neurone in the nerve terminals of the colon.
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PMID:Contractile effect of morphine and related opioid alkaloids, beta-endorphin and methionine enkephalin on the isolated colon from Long Evans rats. 617 Mar 77

Brattleboro rats which lack endogenous vasopressin have been used to study the role of vasopressin as a corticotropin-releasing factor. Plasma ACTH, beta-endorphin, and corticosterone were measured by RIA in male and female Long-Evans and Brattleboro rats under the following conditions: unstressed, after ether stress, after nicotine injection, and after adrenalectomy. A significant reduction in the ACTH, beta-endorphin, and corticosterone responses to the different experimental procedures was observed in the Brattleboro rats. However, in this strain of rats, a significant increase in the release of all three hormones was obtained, suggesting that vasopressin has only a synergistic role in the regulation of their secretion.
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PMID:Adrenocorticotropin, and corticosterone secretion in Brattleboro rats. 628 Sep 88

The effect of catecholamines on plasma levels of immunoreactive ACTH (ACTHi), alpha-MSH (alpha-MSHi), beta-endorphin (beta-ENDi), arginine-vasopressin (AVPi) and of corticosterone (B) was studied in female rats. Intravenous infusion of the specific beta-adrenoceptor-stimulating agent l-isoproterenol in Wistar rats under pentobarbital anesthesia resulted in a dose-dependent (dose range: 10-100 ng/kg . min) increase in plasma B. At higher concentrations, l-isoproterenol also caused a dose-dependent increase in plasma AVPi (dose range: 100-1,000 ng/kg . min). In addition to isoproterenol, also intravenous infusion of l-epinephrine caused a dose-dependent increase of plasma B (dose range: 100-1,000 ng/kg . min), whereas l-epinephrine was without effect on plasma AVPi, even at the highest dose tested (1,000 ng/kg . min). The effect of l-epinephrine or l-isoproterenol on plasma B was associated with a parallel and dose-related increase in plasma ACTHi, beta-ENDi and alpha-MSHi. The increase of plasma ACTHi, B and beta-ENDi in response to l-isoproterenol (300 ng/kg . min) was identical in Wistar, Long Evans and Brattleboro rats (Long Evans rats with a hereditary lack of vasopressin). Also the responses to l-epinephrine (1,000 ng/kg . min) were identical in Wistar and Brattleboro rats. We conclude that vasopressin does not mediate the catecholamine-induced release of ACTH, beta-endorphin and alpha-MSH.
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PMID:Vasopressin is not involved in the catecholamine-induced release of ACTH, alpha-MSH and beta-endorphin from the rat pituitary gland. 631 Apr 30

I.c.v. administration of bacterial endotoxin produced a fever in the Long-Evans rat but not in the Brattleboro rat. Similar administration of arachidonic acid, prostaglandin E2, prostacyclin, dibutyryl cAMP, norepinephrine, morphine and beta-endorphin caused hyperthermia in both Long-Evans and Brattleboro rats. Variable doses of exogenous arginine vasopressin (AVP) when centrally administered with endotoxin caused fever in the Brattleboro rat. It is suggested that AVP may play an important role in the production and release of endogenous pyrogen.
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PMID:Absence of endotoxin-fever but not hyperthermia in Brattleboro rats. 631 28

The effect of beta-endorphin on spatial working memory was examined following microinfusions of beta-endorphin into the medial septal area and central amygdaloid nucleus in Long-Evans male rats. Working memory was assessed by spatial alternation in a T-maze. beta-Endorphin, 250 and 1000 ng/site, respectively, and muscimol, 20 ng/site, were infused into the medial septal area or central amygdaloid nucleus prior to behavioral testing. The hippocampal theta rhythm was examined following intraseptal infusions of beta-endorphin and muscimol. In the medial septal area, beta-endorphin and muscimol impaired choice accuracy and reduced the power of hippocampal theta rhythm. The degree of reduction in the power of hippocampal theta rhythm was correlated with the magnitude of behavioral impairment of choice accuracy in spatial alternation. In the central amygdaloid nucleus, beta-endorphin (1000 ng) and muscimol (20 ng) did not affect choice accuracy. The results suggest that septal, but not amygdaloid, opioid, and GABAergic activity modulate spatial working memory and hippocampal physiology.
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PMID:Opioid modulation of working memory: intraseptal, but not intraamygdaloid, infusions of beta-endorphin impair performance in spatial alternation. 766 81

The long-term consequences of neonatal endotoxin exposure on hypothalamic-pituitary-adrenal axis (HPA) function were assessed in adult female and male Long-Evans rats. At 3 and 5 d of age, pups were administered endotoxin (Salmonella enteritidis, 0.05 mg/kg, i.p.) at a dose that provokes a rapid and sustained physiological response, but with no mortality. As adults, neonatally endotoxin-treated animals exhibited significantly greater adrenocorticotrophic hormone (ACTH) and corticosterone responses to restraint stress than controls. In addition, dexamethasone pretreatment was less effective in suppressing ACTH responses to restraint stress in endotoxin-treated animals than in controls, suggesting decreased negative-feedback sensitivity to glucocorticoids. Neonatal endotoxin treatment elevated resting-state median eminence levels of corticotropin-releasing hormone (CRH) and arginine vasopressin in adult male animals, and arginine vasopressin in both adult males and females. Neonatal exposure to endotoxin also increased CRH mRNA expression in the paraventricular nucleus of the hypothalamus of adult males, with no difference in females. Finally, glucocorticoid receptor density was reduced across a wide range of brain regions in the neonatal endotoxin-treated, adult animals. These data illustrate the interactive nature of immune and endocrine systems during development. It appears that endotoxin exposure during critical stages of development decreases glucocorticoid negative-feedback inhibition of ACTH secretagogue synthesis, thus increasing HPA responsiveness to stress. The implication of these findings is that exposure to gram-negative LPS in early life can alter the development of neural systems which govern endocrine responses to stress and may thereby predispose individuals to stress-related pathology.
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PMID:Neonatal endotoxin exposure alters the development of the hypothalamic-pituitary-adrenal axis: early illness and later responsivity to stress. 782 42

Exposure to endotoxin is known to activate hypothalamic-pituitary-adrenal (HPA) responses in both adult and neonatal animals. We have previously reported that female rat pups exhibit greater HPA responses to endotoxin challenge than males. It is unclear, however, whether observed gender differences at this early age are mediated by gonadal factors. In the present investigation we assessed the effects of neonatal gonadectomy on HPA responses to endotoxin challenge in the developing rat. On the first day of life Long-Evans rat pups were gonadectomized or subjected to sham surgery. On the third day of life the pups were injected i.p. with 0.05 mg/kg Salmonella enteritidis endotoxin. Four hours following injection, trunk blood and tissues were collected for determination of plasma hormones and median eminence corticotropin-releasing hormone (CRH) content. Intact female rat pups were found to exhibit greater plasma adrenocorticotrophic hormone (ACTH) and corticosterone responses to endotoxin challenge compared with male animals. Plasma corticosterone levels, both total and free steroid, were markedly altered by removal of gonads such that responding to endotoxin was elevated in males, while it was reduced in females. In contrast, ACTH responding in male pups was not altered following gonadectomy, whereas female ACTH responses were significantly reduced compared with endotoxin-treated intact controls. CRH levels in the median eminence were reduced following endotoxin challenge to an equivalent extent in both male and female pups and this effect was partially attenuated by the removal of gonadal hormones. These data suggest that sex differences in HPA responses to immune challenge may be mediated at different levels of the HPA axis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sex differences in hypothalamic-pituitary-adrenal responding to endotoxin challenge in the neonate: reversal by gonadectomy. 795 24

The present studies assessed hypothalamic-pituitary-adrenal (HPA) responses following immune activation with endotoxin (i.p.) in three-day old Long Evans rats. Marked plasma corticosterone (B), adrenocorticotrophic hormone (ACTH) responses and biphasic fluctuations in plasma glucose were maximal at a dose of 0.05 mg/kg. HPA responses peaked between 3-5 h following immune challenge and plasma ACTH and B responses were greater in female than in male rat pups. Plasma levels of corticosterone binding globulin (CBG) were reduced in males and substantially increased in females during the peak HPA response. Changes in plasma glucose were biphasic with slight increases when ACTH and B levels were maximal, but hypoglycemia was evident once plasma B levels returned to resting values. Endotoxin challenge reduced median eminence corticotropin-releasing hormone (CRH) levels at times corresponding with elevated HPA activity, and prior i.c.v. injection of the CRH antagonist, alpha-helical CRH, significantly attenuated elevations in plasma ACTH and B. In addition, alpha-helical CRH pretreatment completely blocked endotoxin-induced changes in plasma CBG in both males and females. These findings support the view that endotoxin-induced HPA activation in the neonate may occur via CRH.
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PMID:Hypothalamic-pituitary-adrenal activation following endotoxin administration in the developing rat: a CRH-mediated effect. 798 67

To elucidate the role of arginine vasopressin (AVP) in the development of stress-induced gastric ulcer, the mucosal lesions after restraint and water immersion were examined in Brattleboro strain rats with hereditary hypothalamic diabetes insipidus (DI) and in Long-Evans rats (LE) used as controls. Restrained animals were immersed in water for 2 h, and the size of lesion was expressed as percentage of the lesion area to the total glandular mucosal area, which were defined as ulcer index (UI). In DI rats, UI was significantly higher than in control LE rats, despite the attenuated responses of plasma adrenocorticotropic hormone (ACTH) to stress. Although subcutaneous injection of selective antidiuretic analogue 1-desamino-8-D-AVP did not affect UI, intracerebroventricular (icv) administration of AVP reduced UI in DI rats, and icv administration of V1 antagonist [d(CH2)5Tyr(Me)]AVP elevated UI in LE rats. These results indicate that endogenous AVP plays a role in preventing the formation of gastric ulcers induced by stress via a central V1 receptor. Furthermore, we suggest that elevation of ACTH in plasma is not essential in the development of stress-induced gastric ulcer in rats.
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PMID:Role of endogenous vasopressin in development of gastric ulcer induced by restraint and water immersion. 820 19


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