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)

In homozygous (di/di) Brattleboro rats, pro-opiomelanocortin (POMC) synthesis and processing, and the release of its products, is by definition not under the control of hypothalamic arginine vasopressin (AVP) in contrast with normal rats or heterozygote (di/+) littermates. To explore the role of AVP on these parameters, we have compared homozygotes and heterozygotes in terms of POMC mRNA levels, pituitary content of immunoreactive (ir)-ACTH, ir-beta-endorphin (beta-EP), alpha-melanocyte-stimulating hormone (alpha-MSH) and ir-N-acetyl-EP (NacEP), plasma levels of ir-ACTH and ir-beta-EP, and RP-HPLC profiles of the various forms of ir-alpha-MSH and ir-NacEP. Homozygous rats had immeasurably low levels of hypothalamic ir-AVP, in contrast with their heterozygote littermates; hypothalamic ir-corticotropin releasing factor did not differ between strains. No difference between-strains was seen in levels of POMC mRNA; elevated levels of all pituitary peptides, except ir-ACTH, were found in di/di rats; plasma levels of both ir-ACTH and ir-beta-EP were lower in di/di rats; pituitary ir-alpha-MSH RP-HPLC profiles were similar in both strains, but those for ir-NacEP showed a striking increase in Nac alpha-EP in di/di rats. We interpret these data as evidence for decreased degradation/retarded release of POMC products from the di/di anterior pituitary, for increased processing of POMC products to shorter forms in both anterior pituitary and neuro-intermediate lobe, and thus for a role of AVP in the processing of POMC, as well as POMC synthesis and ACTH/beta-EP release.
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PMID:Post-translational processing of pro-opiomelanocortin in the Brattleboro (di/di) rat pituitary. 285 4

The purpose of this study was to compare the control of adrenocorticotropin (ACTH) and corticosterone secretion in homozygous Brattleboro rats with their syngeneic controls, Long-Evans rats, and with rats of the Wistar strain. Plasma concentrations of ACTH and corticosterone were measured by radioimmunoassay in trunk blood, and corticotropin-releasing factor 41 (CRF-41), arginine vasopressin (AVP), and oxytocin were assayed in hypophysial portal vessel blood. Portal plasma was extracted with methanol for CRF-41 determination, and four different antisera and several different high-performance liquid chromatography (HPLC) systems were used to investigate AVP release. The peripheral plasma concentrations of ACTH and corticosterone were significantly higher in Long-Evans and homozygous Brattleboro than in Wistar rats. This difference was due, at least in part, to an approximately twofold greater release of CRF-41 into hypophysial portal blood of the Long-Evans and Brattleboro compared with Wistar rats. There was no significant difference between the strains in the output of oxytocin into portal blood. While no AVP could be detected in the neural lobe of homozygous Brattleboro rats, a small amount of AVP-like immunoreactivity was detected in unextracted hypophysial portal blood from homozygous Brattleboro rats. However, this AVP-like immunoreactivity was clearly distinct from authentic AVP in several HPLC systems, had no antidiuretic activity, and on gel filtration had a relative molecular mass greater than 5 kD. In contrast, the AVP-like immunoreactivity in hypophysial portal blood from Long-Evans rats co-eluted with authentic AVP in all HPLC systems tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of adrenocorticotropin control in Brattleboro, Long-Evans, and Wistar rats. Measurement of corticotropin-releasing factor, arginine vasopressin, and oxytocin in hypophysial portal blood. 285 6

Rat anterior pituitary quarters or acutely dispersed rat anterior pituitary cells were incubated in vitro, and the release of dynorphin A1-13-like immunoreactivity (Dyn A1-13-IR) into the incubation medium was studied. Addition of LHRH led to a concentration-dependent enhancement of the release of Dyn A1-13-IR with a maximum secretory rate which was about 4-fold higher than basal secretion. Dyn A1-13-IR was released by LHRH concomitantly with LH and FSH, and the concentration-response relationships as well as the time course were virtually identical. Gel filtration and HPLC revealed a single peak of Dyn A1-13-IR, with an apparent mol wt of about 6000. In addition to Dyn A1-13-IR, alpha-neo-endorphin-like immunoreactivity was released by LHRH. The LHRH-stimulated release of Dyn A1-13-IR was mimicked by the LHRH analog D-Ala6,des-Gly10-LHRH ethylamide and blocked in a competitive manner by the LHRH antagonist D-pGlu1,D-Phe2,D-Trp3,6-LHRH. Addition of TRH (5 microM), rat corticotropin-releasing factor (100 nM), arginine vasopressin (1 microM), or synthetic human pancreatic GH-releasing hormone (10 nM) produced no effect on Dyn A1-13-IR release. An extract of the rat medial basal hypothalamus stimulated the release of Dyn A1-13-IR and beta-endorphin-like immunoreactivity, and the former, but not the latter, effect was blocked by the LHRH antagonist D-pGlu1,D-Phe2,D-Trp3,6-LHRH. These results demonstrate that dynorphin-like material and other proenkephalin B-derived peptides are released concomitantly with LH and FSH from rat adenohypophysis in vitro upon activation of LHRH receptors. This may indicate that proenkephalin B-derived peptides coexist with LH and/or FSH in at least some gonadotrophs of the normal rat anterior pituitary gland.
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PMID:Corelease of dynorphin-like immunoreactivity, luteinizing hormone, and follicle-stimulating hormone from rat adenohypophysis in vitro. 286 8

As a first step toward assessing the status of brain neuropeptide systems that may be involved in Alzheimer's disease (AD), the cerebrospinal fluid (CSF) concentrations of the neuropeptides arginine vasopressin, somatostatin, oxytocin, and beta-endorphin were measured in patients with AD, normal elderly subjects, and normal young subjects. The plasma arginine vasopressin level was also measured in the three groups. The CSF arginine vasopressin level was significantly lower in patients with AD than in either elderly or young normal subjects, but oxytocin and beta-endorphin levels did not differ between groups. The CSF osmolarity also did not differ between groups. The plasma arginine vasopressin level did not significantly differ between groups, but high plasma arginine vasopressin values were absent in the patients with AD. The CSF somatostatin level was significantly lower in patients with AD than in normal elderly persons, but it did not differ in young normal subjects. These results suggest that central vasopressinergic activity may be decreased in AD and confirm reports of low CSF somatostatin levels in AD.
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PMID:Cerebrospinal fluid vasopressin, oxytocin, somatostatin, and beta-endorphin in Alzheimer's disease. 286 44

Adrenocorticotropic hormone (ACTH)1-24, ACTH4-10, corticosterone (CS) or arginine vasopressin (AVP) was administered subcutaneously to one day-old chicks immediately after learning a single trial passive avoidance task. Chicks were pretreated with 2 mM KC1 or 4 mM monosodium glutamate 5 min before learning. With KC1 or monosodium glutamate alone, no evidence of memory was observed on retention tests carried out as early as 5 min and as late as 24 h postlearning. However, the addition of ACTH1-24, ACTH4-10 or AVP to KC1-pretreated animals yielded normal retention levels up till 10 min, 10 min and 20 min after learning, respectively. Similar results were obtained with ACTH1-24 and AVP given to glutamate-pretreated birds. CS had no effect on KC1- or glutamate-induced amnesia. The calcium channel blocker, lanthanum chloride, also inhibited the formation of short-term memory, with amnesia still present as late as 24 h following learning. ACTH1-24, but not CS or AVP, yielded normal retention levels until 10 min postlearning in the presence of lanthanum chloride. Thus ACTH1-24 and AVP can overcome KC1 or glutamate inhibition of STM formation but will not prevent subsequent amnesia. The mechanisms underlying this action of ACTH1-24 and AVP are different. The possibility that the effect of ACTH1-24 is related to the role of calcium in STM formation is explored.
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PMID:Effect of stress-related hormones on short term memory. 286 68

The hypothalamus provides a major projection to the spinal cord that innervates primarily lamina I of the dorsal horn and the sympathetic and parasympathetic preganglionic cell columns. We have examined the chemical organization of the neurons that contribute to this pathway by using combined retrograde transport of fluorescent dyes and immunohistochemistry for 15 different putative neurotransmitters or their synthetic enzymes. Our results demonstrate that 5 cytoarchitectonically distinct cell groups in the hypothalamus contribute to the spinal projection and that each has its own predominant chemical types. In the paraventricular nucleus, substantial numbers of hypothalamo-spinal neurons stain with antisera against arginine vasopressin (25-35%), oxytocin (20-25%), and met-enkephalin (10%). About 25% of the neurons with spinal projections in the retrochiasmatic area stain with an antiserum against alpha-melanocyte-stimulating hormone. Nearly 100% of the hypothalamo-spinal neurons in the tuberal lateral hypothalamic area stain with this same antiserum, but these cells do not stain for other proopiomelanocortin-derived peptides, and so probably contain a cross-reacting peptide. This population must be distinguished from an adjacent cell group, in the perifornical region, where many spinal projection neurons stain with antisera against dynorphin (25%) or atrial natriuretic peptide (20%). Finally, in the dorsal hypothalamic area as many as 55-75% of the neurons with spinal projections are dopaminergic, on the basis of their staining with an antiserum against tyrosine hydroxylase. These 5 neurochemically distinct projections from the hypothalamus to the spinal cord are discussed in the context of their possible functional significance.
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PMID:Neurochemical organization of the hypothalamic projection to the spinal cord in the rat. 290 38

The role of opioids in the regulation of arginine vasopressin release from the posterior pituitary is a subject of controversy. In the present study, we examined the effects of central administration of met-enkephalin, leu-enkephalin, the enkephalin analogue FK-33824, and the opiate antagonist naloxone, and the effects of systemic administration of met-enkephalin and FK-33824 on AVP secretion in conscious normal sheep. Intracerebroventricular infusion of FK-33824 significantly increased the plasma concentration of immunoreactive AVP in a dose-dependent manner, but met-enkephalin, leu-enkephalin and naloxone failed to change plasma concentration of AVP. Intravenous infusion of met-enkephalin and FK-33824 also failed to change plasma concentration of AVP. The opiate antagonist naloxone given both centrally and systemically attenuated the increase in plasma concentration of AVP induced by FK-33824. We conclude that basal AVP release is stimulated by central administration of FK-33824.
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PMID:Central effect of the enkephalin analogue FK-33824 on vasopressin secretion in conscious sheep. 292 39

We have investigated the role of adrenal steroids and the opiates in regulating arginine vasopressin (AVP) secretion into the pituitary stalk blood of the rat. The portal plasma concentration of AVP in urethane-anesthetized male rats was 532 +/- 68 pg/ml (mean +/- SEM), while the peripheral plasma AVP concentration in intact urethane-anesthetized rats was 20.7 +/- 5.7 pg/ml. Column chromatography on Sephadex G-25 of an extract of a pool of portal plasma revealed that the material being assayed comigrated with synthetic AVP. Bilateral adrenalectomy (ADX) 5 days before the collection of portal blood elevated portal plasma AVP concentrations approximately 6-fold (655 +/- 124 pg/ml in controls vs. 4090 +/- 504 pg/ml in adrenalectomized animals). Dexamethasone administration (15 micrograms/kg X day) for 5 days prevented the ADX-induced increase in portal plasma AVP concentrations without significantly changing portal plasma AVP concentrations in intact rats. Portal plasma concentrations of beta-endorphin were not changed by ADX or dexamethasone treatment. The iv infusion of morphine sulfate (3 mg/kg) dramatically decreased the concentration of AVP in the portal plasma of the rat (501 +/- 101 pg/ml before morphine vs. 185 +/- 50 pg/ml after morphine). The inhibitory effect of morphine was reversed by naltrexone (1.0 mg/kg), whereas naltrexone alone did not alter AVP secretion. Morphine administration also decreased systemic plasma AVP concentrations in urethane-anesthetized rats (27.1 +/- 6.6 pg/ml in controls vs. 3.3 +/- 1.3 pg/ml in morphine-treated rats). Naltrexone treatment reversed this effect. These results suggest that AVP secretion into pituitary stalk blood is under the inhibitory influence of the adrenal steroids, and the increased concentration of AVP found in portal blood may be partially responsible for the elevated levels of ACTH after ADX. Furthermore, morphine-induced activation of the pituitary-adrenal axis is apparently independent of hypothalamic AVP secretion.
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PMID:The concentration of arginine vasopressin in pituitary stalk plasma of the rat after adrenalectomy or morphine. 293 37

Plasma cortisol, beta-endorphin immunoreactivity (PBEir) and arginine vasopressin (AVP) responses during and after the continuous infusion of fentanyl or alfentanil were studied in 19 patients undergoing coronary artery bypass grafting (CABG). Plasma cortisol concentration decreased significantly in both groups during the anaesthesia and surgery before cardiopulmonary bypass (CPB); an increase was evident during CPB in both groups, but a statistically significant increase was not observed during the rest of the study, including the awakening from anaesthesia. PBEir increased with both opiates immediately after initiation of CPB and remained so during the rest of the study. There were no significant changes in plasma AVP concentrations during anaesthesia and surgery. After discontinuation of opiate infusions, an increase in AVP concentration commenced earlier in the alfentanil group than in the fentanyl group. At awakening from anaesthesia, a significant correlation was observed between log plasma AVP concentration and systemic vascular resistance. It is concluded that, with continuous fentanyl and alfentanil infusions in a total dose relationship of 1:13 in patients undergoing CABG, cortisol and AVP responses to surgery and CPB can be suppressed. However, during recovery from anaesthesia, the attenuating effect of alfentanil seems to wear off more rapidly than that of fentanyl. PBEir response to CPB and emergence from anaesthesia could not be prevented with either analgesic.
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PMID:Continuous infusion of fentanyl or alfentanil for coronary artery surgery. Effects on plasma cortisol concentration, beta-endorphin immunoreactivity and arginine vasopressin. 294 13

Synthesis and secretion of POMC-derived peptides appear to be differentially regulated in the anterior pituitary (AP) and neurointermediate lobe (NIL). In the AP, glucocorticoids inhibit, and CRF and arginine vasopressin stimulate, synthesis of POMC and release of immunoreactive (ir)-beta-endorphin (beta EP); in the NIL, synthesis and release of POMC and its derivatives are under tonic inhibitory dopaminergic control. There is, however, evidence for some overlap of these control mechanisms under certain circumstances. In the present study we have used specific RIA and Northern blot analysis to examine the effects of chronic treatment with dopaminergic agents and dexamethasone (DM) (both alone and in combination) on AP and NIL content of ir-beta EP and POMC messenger RNA (mRNA), and/or hypothalamic ir-arginine vasopressin and ir-CRF content. In the NIL, the dopamine agonist bromocriptine reduced and the antagonist haloperidol raised both POMC mRNA and ir-beta EP content. Long term DM treatment did not alter NIL ir-beta EP content in the intact rat, but increased levels of POMC mRNA. DM abolished the haloperidol-induced increase in NIL ir-beta EP content but further increased the haloperidol-induced rise in POMC mRNA. DM treatment lowered both ir-beta EP and POMC mRNA in the AP as well as lowering levels of hypothalamic ir-CRF. In DM-treated rats, haloperidol partially restored AP ir-beta EP and POMC mRNA to control untreated levels. These findings further support the proposition that both dopaminergic agents and glucocorticoids can modulate POMC mRNA levels and/or tissue content of ir-beta EP in both the NIL and AP of the rat. The effects of DM on the NIL, both alone or with haloperidol, suggest that glucocorticoids may have both direct and indirect effects on POMC gene expression in this tissue.
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PMID:Concomitant dopaminergic and glucocorticoid control of pituitary proopiomelanocortin messenger ribonucleic acid and beta-endorphin levels. 295 68


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