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)

Cerebrospinal fluid hormones, monoaminergic metabolites, and dynorphin A (1-8 sequence) were examined in 43 children with severe, primary obsessive-compulsive disorder. Cerebrospinal fluid levels of 5-hydroxyindoleacetic acid were positively correlated with one of eight obsessive-compulsive disorder severity ratings and three of seven measures of improvement following 5 weeks of treatment with clomipramine hydrochloride. Arginine vasopressin concentration was significantly and negatively correlated with several ratings of obsessive-compulsive disorder symptom severity, while oxytocin concentration was positively correlated with depressive symptoms. The ratio of arginine vasopressin to oxytocin was also negatively correlated with obsessive-compulsive disorder and depressive symptoms. Comorbid affective disorder was associated with decreased arginine vasopressin concentrations, while concomitant anxiety disorder was associated with increased oxytocin. Dynorphin A (1-8 sequence), homovanillic acid, corticotropin, 3-methoxy-4-hydroxyphenylglycol, and corticotropin releasing hormone were not significantly related to obsessive-compulsive disorder symptoms. These results seem to indicate that arginine vasopressin may be related to obsessive-compulsive disorder symptom severity, while 5-hydroxyindoleacetic acid might be associated with drug response.
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PMID:Cerebrospinal fluid neurochemistry in children and adolescents with obsessive-compulsive disorder. 137 Jan 97

The fasting plasma levels of 10 vasoactive regulatory peptides were measured by radioimmunoassay in 23 stable patients with chronic renal failure receiving regular hemodialysis treatment (RDT) and compared with those of healthy controls. The plasma concentrations of arginine vasopressin, atrial natriuretic peptide, beta-endorphin, methionine-enkephalin, motilin, neuropeptide Y, substance P, and vasoactive intestinal peptide were increased. The plasma level of calcitonin gene-related peptide was not statistically different from that of the controls. The plasma concentration of gamma 2-melanocyte-stimulating hormone was lowered in the RDT-patients. The arterial blood pressure correlated with the plasma levels of motilin and neuropeptide Y. We conclude that patients with chronic renal failure receiving RDT have increased concentrations of 8 out of 10 measured vasoactive regulatory peptides. The elevated levels of vasoactive peptides may contribute to the adaptation of the cardiovascular system to impaired renal function.
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PMID:Plasma levels of vasoactive regulatory peptides in patients receiving regular hemodialysis treatment. 137 31

Immunocytochemical localization of neuropeptides (beta-endorphin, substance P, arginine vasopressin, oxytocin), pituitary hormones (adrenocorticotropin, prolactin, growth hormone, follicle stimulating hormone (FSH), gonadal inhibin, gastrin, and human chorionic gonadotrophin (hCG)) was carried out in marmoset testis during development. Both intensity of immunostaining and distribution of these peptides in testicular compartments viz. seminiferous tubules and Leydig cells changed dramatically during development. In vitro biosynthesis of inhibin and FSH was increased by hCG, whereas prolactin (5 micrograms) and prostatic inhibin peptide suppressed the synthesis of these hormones.
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PMID:Immunocytochemical localization of bioregulatory peptides in marmoset testes. 138 Feb 34

Relatively little is known about the regulation of secretion of hypothalamic beta-endorphin, the potent opioid that is believed to play a variety of physiological roles in brain. Previous work has shown that arginine vasopressin (AVP), which acts in brain primarily via activation of the phosphoinositol (PI) second messenger system, stimulates secretion of hypothalamic beta-endorphin. To test the hypothesis that activators of protein kinase C (PKC), which is activated following PI hydrolysis, stimulates secretion of beta-endorphins from hypothalamus, we studied the separate effects of stimulators of PKC including phorbol ester 12-myristate-13-acetate (PMA) and 1-oleolyl-2-acetyl glycerol (OAG- a diacyl glycerol analogue) on secretion of immunoreactive (IR-) beta-endorphin (measured by RIA) from dissociated fetal rat hypothalamic cell cultures. We also studied AVP and angiotensin II (Ang II), hypothalamic peptides which activate the PI second messenger pathway, and interactions of PMA and forskolin (FSK), an activator of the cyclic AMP/protein kinase A (PKA) pathway. PMA, OAG, AVP, and Ang II stimulated IR-beta-endorphin secretion. The stimulatory effect of both PMA and FSK on IR-beta-endorphin secretion was greater than that of PMA or FSK alone and was essentially additive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protein kinase C activators stimulate beta-endorphin secretion from hypothalamic cells. 142 53

In addition to their characterizing secretory products, both magnocellular and parvocellular neurosecretory neurons are now known to express other neuroactive substances. Parvocellular neurons that make corticotropin-releasing factor (CRF) for example are capable of synthesizing at least seven neuropeptides. Some of these, like arginine vasopressin (AVP), interact with CRF at the level of the anterior pituitary to promote corticotropin secretion, and, like CRF, are regulated negatively by glucocorticoids and positively by at least some stressors. others are inert in these two contexts but are responsive to various challenges. Magnocellular neurosecretory oxytocin- and AVP-containing neurons are capable of producing similarly broad and distinctive complements of neuroactive principles. These are typically expressed at levels far lower than those of the nonapeptides, suggesting local modulatory effects on oxytocin and/or AVP secretion at the level of the posterior lobe. Differential regulation of coexisting molecules within magnocellular neurons by systemic challenges and steroid hormones has also been described. Secretory products of magnocellular neurons may gain access to the anterior pituitary via exocytotic release at the level of the median eminence or through vascular links between the posterior and anterior lobes, suggesting another form of 'co-localization' by which the two neurosecretory cell types may interact in the control of stress and perhaps other pituitary-mediated responses.
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PMID:Co-localization of neuroactive substances in the endocrine hypothalamus. 142 23

The purpose of this study is to clarify the central mechanism of food-associated circadian oscillation whereby the prefeeding peak of plasma corticosterone was generated. Adults male rats were subjected to restricted daily feeding in which rats had free access to food at a fixed time of day. The developmental process, the oscillatory nature and the neuroendocrine control of the prefeeding corticosterone peak were investigated. The results were as follows: 1) The prefeeding corticosterone peak was established about one week after the start of restricted feeding. 2) The prefeeding peak persisted for at least 13 days even after the feeding schedule was terminated. 3) Corticotropin releasing hormone in the paraventricular nucleus (PVN) and the lower part of medial basal hypothalamus (MBH) decreased prior to daily feeding and increased postprandially under the restricted feeding. 4) Under restricted daily water supply with free access to food the prefeeding corticosterone peak was not as marked as under the restricted feeding. 5) Plasma arginine vasopressin (AVP) seemed not be involved in the generation of prefeeding corticosterone peak. 6) The prefeeding corticosterone peak failed to appear in the VMH-isolated rats in the dynamic phase, while it appeared in the static phase. These results indicate that the prefeeding corticosterone peak is regulated by an oscillatory mechanism, but are not consistent with the hypothesis that VMH is a site of the oscillation. The present results suggest that the energy state influences the expression of the prefeeding corticosterone peak.
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PMID:[The neuroendocrine regulation of plasma corticosterone rhythm in rats]. 155 56

In this study, we examined the effect of passive immunization of endogenous corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) on hypoglycemia-induced adrenocorticotropic hormone (ACTH) secretion and determined proopiomelanocortin messenger RNA (POMC mRNA) levels in the anterior pituitary as well as hypothalamic CRF mRNA levels in pentobarbital anesthetized rats. The response of plasma ACTH to hypoglycemia was partially inhibited by the administration of CRF-antiserum (CRF-As) or AVP-antiserum (AVP-As) alone, but was found to be completely abolished by the administration of CRF-As + AVP-As as compared to the response in normal rabbit serum-treated rats. The hypoglycemia-induced POMC mRNA level in the anterior pituitary was completely inhibited by the administration of CRF-As alone and CRF-As + AVP-As, but was not inhibited by AVP-As alone as compared to the response in normal rabbit serum-treated rats. The administration of CRF-As and/or AVP-As did not affect hypoglycemia-induced CRF mRNA levels in the hypothalamus. These results indicate that the synergistic effect of CRF and AVP is important for hypoglycemia-induced ACTH secretion, but CRF is essential and indispensable for hypoglycemia-induced POMC gene expression in the anterior pituitary (AP).
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PMID:The role of corticotropin-releasing factor and vasopressin in hypoglycemia-induced proopiomelanocortin gene expression in the rat anterior pituitary gland. 162 18

Although exposure to arginine vasopressin (AVP) has been reported to induce anterior pituitary corticotrophs to bind and become responsive to corticotropin-releasing factor (CRF), the identity of these inducible CRF target cells is unknown. Such cells may themselves be the AVP-responsive corticotrophs or other cells that become CRF targets secondary to a paracrine signal from AVP target cells. The present study used a cytotoxin (Cx), specific for CRF target cells, that eliminates responses of treated cells to a subsequent challenge with CRF but leaves responses to AVP intact. We hypothesized that, if AVP target corticotrophs themselves become CRF targets, then the addition of AVP during treatment with Cx should render these cells susceptible to the cytotoxin and should eliminate the response to subsequent AVP as well. Ovine pituitary cells were chosen for the study because they respond more robustly than rat cells to AVP. Pretreatment of ovine pituitary cells with Cx (400 pM) or Cx plus AVP (10 nM) eliminated the adrenocorticotropic hormone (ACTH) secretory response to CRF (10 nM), as assessed 3 days later. Cx alone also reduced the secretory response to AVP from 23.9 +/- 3.4 to 11.5 +/- 1.9 ng ACTH/3 h (P less than 0.05). However, pretreatment with AVP (10 nM) plus Cx caused no further reduction in the secretory response to AVP (10.1 +/- 2.6 ng ACTH/3 h). These data suggest that, if AVP induces erstwhile non-CRF target cells to become CRF targets, then these induced cells are not themselves initially AVP target corticotrophs.
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PMID:Effect of AVP on susceptibility of ovine pituitary cells to a cytotoxic analogue of CRF. 164 71

The gonadal axis is thought to modulate adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and plasma renin activity (PRA) responses to stimuli in several species. These experiments were designed to compare the responses to hypotension in chronically ovariectomized ewes and intact ewes. The ewes were infused with nitroprusside at rates of 5, 10, or 15 micrograms.kg-1.min-1 or infused with vehicle for 10 min. The response to 15 micrograms.kg-1.min-1 was also tested with or without treatment with 10 mg of dexamethasone 2 h before nitroprusside. Blood samples were collected before and at 5, 10, 15, 20, and 30 min after the start of the infusion for measurement of plasma ACTH, AVP, and PRA. In both groups of animals there were significant responses to hypotension. There was a significant effect of ovariectomy on ACTH, AVP, and PRA responses. ACTH and PRA responses were lower in the ovariectomized ewes; AVP responses were increased in the ovariectomized ewes. Administration of dexamethasone inhibited ACTH responses and did not inhibit PRA responses in both groups of ewes. Administration of dexamethasone did not inhibit the AVP response in the intact ewes but did reduce the response in the ovariectomized ewes.
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PMID:Effect of ovariectomy on vasopressin, ACTH, and renin activity responses to hypotension. 165 Jan 46

Corticosteroid type I and II receptors mediate the negative feedback effects of these hormones at various central nervous system sites involved in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis. To examine the effects of chronic treatment with dexamethasone (DEX), a type 2 receptor agonist, on the regulation of this axis, male Sprague-Dawley rats weighing 200-250 g were given daily injections of DEX for 1,2,3, and 4 weeks or were treated with a subcutaneously implanted DEX-releasing minipump for one week. At the end of treatment, the animals were weighed and brains and truncal blood were collected. Daily intermittent DEX treatment reduced the body weight of the rats in a time-dependent fashion, but had little or no effect on their wet brain weight. Plasma ACTH and corticosterone, measured by RIA, were fully suppressed after one week of intermittent treatment and did not show any further reduction in rats treated for longer periods. In these animals, the content of immunoreactive corticotropin-releasing hormone (iCRH), arginine vasopressin (AVP), ACTH and beta-endorphin (beta-EP) in the hypothalamus, hippocampus, cerebral cortex and cerebellum and pituitary ACTH content did not show any difference compared to vehicle-treated rats. In contrast, continuous DEX treatment increased iCRH content in the cortex, reduced AVP content in the cerebellum, increased ACTH content in the hippocampus, decreased ACTH and beta-EP content in the hypothalamus, and reduced pituitary ACTH content. Hypothalami explanted from rats treated with DEX for one week released lower basal amounts of iCRH in vitro and did not respond to a maximally stimulatory concentration of serotonin (5-HT), a known CRH secretagogue. Continuous DEX administration suppressed also potassium chloride-induced iCRH release. Interestingly, hypothalami explanted from rats receiving daily injection of vehicle, but not from unhandled, untreated controls, did not respond to 5-HT with an increase of iCRH release in vitro. In conclusion, prolonged and continuous, but not intermittent, administration of DEX had a strong effect on brain neuropeptide content. Both regimens of DEX reduced the hypothalamic iCRH responsiveness to stimuli in vitro. Chronic handling also decreased the responsiveness of the hypothalamus to a stimulatory neurotransmitter and may confound the interpretation of data pertinent to inhibitory mechanisms.
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PMID:Hypothalamic and suprahypothalamic effects of prolonged treatment with dexamethasone in the rat. 165 Aug 4


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