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)

Acrolein was examined as an alternative fixative to formaldehyde for immunocytochemical localization of neuropeptides in the rat brain. A brief (5 min) vascular perfusion with a 5% acrolein solution allowed the identification of thyrotropin-releasing hormone (TRH), vasoactive intestinal peptide (VIP), somatostatin (SRIF), neurotensin (NT), methionine enkephalin (Menk), adrenocorticotropic hormone (ACTH), tyrosine hydroxylase (TH), and luteinizing hormone-releasing hormone (LHRH) in fibers and perikarya within the central nervous system of the rat using the peroxidase-antiperoxidase (PAP) technique. Acrolein appears to be particularly valuable for immunocytochemistry, as it 1) stabilizes heterogeneous peptides and proteins rapidly and effectively, 2) retains antigenicity, and 3) preserves morphological detail.
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PMID:Acrolein: a fixative for immunocytochemical localization of peptides in the central nervous system. 618 5

The effects of vasoactive intestinal peptide (VIP) and several other peptides have been examined on cyclic AMP accumulation in intact pieces and isolated horizontal cells of the teleost (carp) retina. VIP was the most effective peptide examined, inducing a dose-related response, and an approximately fivefold increase in cyclic AMP production when used at a concentration of 10 microM. Porcine histidine isoleucine-containing peptide and secretin, peptides structurally related to VIP, also stimulated cyclic AMP accumulation, but at concentrations of 10 microM induced responses which were only approximately 40% and 10%, respectively, of the response observed with 10 microM VIP. In contrast, several other peptides, including glucagon, neurotensin, somatostatin, luteinizing hormone-releasing hormone, alpha-melanocyte-stimulating hormone, cholecystokinin octapeptide26-33, gastrin-releasing peptide, thyrotropin-releasing hormone, and VIP10-28 were totally inactive. The response to 10 microM VIP was not antagonized by several dopamine antagonists, indicating the presence of a population of specific VIP receptors coupled to adenylate cyclase, distinct from the population of dopamine receptors coupled to adenylate cyclase also known to be present in this tissue. Finally, experiments involving the use of fractions of isolated horizontal cells indicate that these neurons possess a population of VIP receptors coupled to cyclic AMP production which would appear to share a common pool of adenylate cyclase with a population of similarly coupled dopamine receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vasoactive intestinal peptide and other peptides on cyclic AMP accumulation in intact pieces and isolated horizontal cells of the teleost retina. 619 61

Primary cultures of neonatal murine brain have been reported to express multiple receptors that regulate adenylate cyclase activity. Since for the most part these results were obtained with mixed cell cultures, it has been difficult to define receptor profiles for specific cell types. With this concern in mind a series of studies has been initiated designed to identify specific receptors present on highly purified, immunocytochemically defined astroglia derived from the cerebral cortices of neonatal rats. In this study the capacity of a variety of peptide hormones to regulate cyclic AMP metabolism in these cells was examined. Fibroblasts derived from the meninges represent a predictable source of contamination in primary CNS culture. Thus, to assign more clearly specific receptors to the astroglial cell population, receptor-mediated regulation of cyclic AMP accumulation was also examined in fibroblasts. Cyclic AMP accumulation in astroglia was stimulated by catecholamines (acting at beta 1-adrenergic receptors), prostaglandin E1, vasoactive intestinal polypeptide, alpha-melanocyte-stimulating hormone, and adrenocorticotropin. Bombesin, luteinizing hormone-releasing hormone, neurotensin, thyrotropin-releasing hormone, somatostatin, secretin, and vasopressin did not significantly increase cyclic AMP levels in these cultures. Catecholamines, acting at alpha 2-adrenergic receptors, and somatostatin inhibited agonist-stimulated cyclic AMP accumulation. In meningeal cell cultures catecholamines (acting at beta 2- and alpha 2-adrenergic receptors) and prostaglandin E1 regulated cyclic AMP levels. However, vasoactive intestinal peptide did not stimulate and somatostatin did not inhibit cyclic AMP accumulation in these cells.
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PMID:Regulation of cyclic AMP accumulation by peptide hormone receptors in immunocytochemically defined astroglial cells. 620 41

Severe symptomatic hypoglycemia (serum glucose level, 24 mg/dL) developed in a 23-year-old, 147.3-cm-tall woman during her late second and third trimesters of pregnancy. Endocrine studies disclosed insulin levels less than 2 microU/mL; growth hormone level less than 3 ng/mL; and cortisol level less than 1 microgram/dL. Hydrocortisone therapy corrected her hypoglycemia, and she was delivered of a healthy female infant. Postpartum, her evaluation included normal thyroid function studies, a normal thyroid-stimulating hormone response to protirelin (thyrotropin-releasing hormone), normal serum and urine gonadotropin levels, normal serum prolactin, normal sella turcica tomograms, and a normal EMI brain scan. Urine 17-hydroxycorticosteroids increased during a four-day cosyntropin infusion, but failed to rise after metyrapone administration. The growth hormone level failed to rise after stimulation with levodopa and propranolol administration. The patient was believed to have idiopathic partial hypopituitarism, with hypoglycemia being due to adrenocorticotropic hormone (ACTH) and growth hormone deficiency and the drain of maternal glucose by the fetus. It is suggested that pregnant women with symptomatic hypoglycemia be treated with glucocorticoids while awaiting the results of their endocrine evaluation.
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PMID:Hypoglycemia in pregnancy. Occurrence due to adrenocorticotropic hormone and growth hormone deficiency. 624 99

Ovariectomized female rats were implanted with estradiol containing silastic implants to induce constant circulating levels of the steroid, and sacrificed every 2 h in order to determine neuroendocrine rhythms. Under these conditions, we observed very marked circadian fluctuations in the hypothalamic concentrations of corticotropin-releasing factor (CRF), luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH), and in plasma levels of adrenocorticotropin (ACTH), corticosterone, luteinizing hormone (LH) and prolactin; the amplitude of the prolactin cycle was in particular much higher than in non-chronically estrogenized animals. The daily variation in CRF, ACTH and corticosterone showed significant rank correlations. Changes in hypothalamic content of LHRH and TRH were biphasic; the increase observed during the light period was abruptly interrupted by a depletion episode, coincident with the period of maximal LH and prolactin secretion, respectively. The initial phase of ACTH, LH and prolactin increments occurred between 11.00 and 15.00 h, and was relatively well synchronized. The steepest rise in ACTH and prolactin occurred at the same time, and preceded that of LH by a constant lag of about 2 h. After that initial period, secretion kinetics of the three hormones followed an independent pattern. The data suggest that increased secretion of several hormones results from activation of neural mechanisms occurring within a limited period of the 24-hour cycle.
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PMID:Temporal relationships between the circadian rhythmicity in plasma levels of pituitary hormones and in hypothalamic concentrations of releasing factors. 624 69

Ethanol (2.0-5.0 g/kg, IP) caused a dose-related impairment of the aerial righting reflex of mice 60 min after injection. Ethanol (3.5 g/kg, IP) given simultaneously with neurotensin (30 micrograms, IC), bombesin (30 micrograms, IC) or beta-endorphin (20 micrograms, IC) caused a greater impairment of the reflex than ethanol alone. Simultaneous treatment with ethanol (4.0 g/kg, IP) and thyrotropin-releasing hormone (TRH, 3.0-30 micrograms, IC) caused less impairment of this measure than ethanol alone. None of the peptides altered the height of aerial righting when administered alone, or when administered with ethanol no peptide altered blood or brain ethanol content. Unexpectedly, TRH (20 and 40 mg/kg, IP) potentiated the action of ethanol by increasing punished licking in water-deprived rats, rather than antagonizing this acute action of ethanol. Like ethanol (1.0 and 2.0 g/kg, IP), beta-endorphin (100 micrograms, IC) suppressed ethanol-withdrawal tremor and audiogenic-seizure susceptibility in ethanol-dependent rats. beta-Endorphin (1 microgram) and bombesin (10 and 30 micrograms, IC) reduced only audiogenic-seizure susceptibility. TRH (10-100 micrograms, IC, or 1-40 mg/kg, IV) and neurotensin (10-100 micrograms, IC) had no effect on these ethanol-withdrawal signs. These findings suggest that centrally active peptides may play a role in certain acute and chronic actions of ethanol. Because TRH, neurotensin, bombesin and beta-endorphin do not alter all actions of ethanol in the same way, an interaction of ethanol with many functionally independent neuronal circuits is suggested.
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PMID:Modification of the actions of ethanol by centrally active peptides. 626 62

Effects of intracerebroventricular administration of beta-endorphin, thyrotropin-releasing hormone (TRH), cholecystokinin octapeptide (CCK-8), non-sulfated CCK-8 (CCK-8-NS) and caerulein on body shaking behavior were observed in rats. CCK-8 and its related peptides produced only a small increase in the number of body shakes, while TRH had the striking effect of stimulating body shakes, this increase being markedly suppressed by simultaneous administration of beta-endorphin. Moreover, the suppressive effect of beta-endorphin on TRH-induced body shakes was antagonized by simultaneous administration of caerulein and CCK-8. The body shakes induced by ice-water immersion were also reduced by beta-endorphin, this beta-endorphin effect being partly antagonized by caerulein and CCK-8.
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PMID:Effects of beta-endorphin, thyrotropin-releasing hormone and cholecystokinin on body shaking behavior in rats. 629 91

Neurotensin (NT) and bombesin, which are heterogeneously distributed in both brain and gastrointestinal tissue of several mammalian species, inhibit the formation of stress-induced gastric ulcers in rats. Many other endogeneous neuropeptides have also been reported to be present in brain and gastrointestinal tissue. The present study was conducted to evaluate the effect of some of these peptides on the development of cold-restraint stress (CRS)-induced gastric ulcers in rats. In addition, the effect of thyrotropin-releasing hormone (TRH), which antagonizes many of the CNS effects of NT, was investigated to determine whether this tripeptide antagonizes the cytoprotective effect of NT in this CRS model. All peptides were initially administered intracisternally (ic) in doses equimolar to 30 micrograms NT. As previously reported, NT (30 micrograms, ic) completely prevented the development of gastric ulcers in rats exposed to three hours of CRS. Bombesin, beta-endorphin, substance P, and somatostatin also exhibited cytoprotective activity. Several other peptides studied in the CRS model exerted no significant effects on the development of gastric ulcers; these included cholecystokinin octapeptide, gastrin, leu-enkephalin, met-enkephalin, and bradykinin. Two peptides, vasoactive intestinal polypeptide and TRH, significantly increased the severity of gastric ulcerations. The cytoprotective effect of NT was dose dependent. In contrast, lower doses of beta-endorphin, substance P, and somatostatin were cytoprotective whereas higher doses were not. Finally, concomitant ic injections of TRH antagonized the cytoprotective effects of NT and bombesin, but not that of beta-endorphin. The present results suggest that certain brain peptides may participate in modulating the gastric mucosal barrier, thereby increasing or decreasing its vulnerability to stress-induced lesions.
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PMID:The effect of centrally administered neuropeptides on the development of stress-induced gastric ulcers in rats. 630 95

Injury to the spinal cord is associated with large increases in plasma beta-endorphin immunoreactivity. To investigate the effect on vesical function of thyrotropin-releasing hormone (TRH), 13 patients with spinal injury were studied during the spinal shock phase. In seven of them (Group A), after basal cystometry together with anal sphincter electromyography (EMG), 1 mg of TRH was administered intravenously as a bolus dose, followed by 1 mg infused over 5 minutes. After the administration of the bolus dose of TRH, cystometry + EMG was repeated (Study I). These seven cases received TRH 1 mg intravenously 12 hourly for the next three days. On day 4, after basal cystometry + EMG, TRH was administered as above and the urodynamic study was repeated (Study II). Detrusor pressure (Pdct) with bladder filled to 800 ml (or upto tolerance) and bladder compliance were noted. Six cases underwent study I alone and received normal saline instead of TRH (Group B). After TRH in group A, the mean (+/- SE) Pdct increased by 10 +/- 3 cm H2O (p less than 0.05) in study I and by 10 +/- 3 cm H2O (p less than 0.05) in study II whereas the mean compliance decreased by 37 +/- 20 ml/cm H2O (NS) in study I and by 44 +/- 18 ml/cm H2O (p less than 0.05) in study II. In group B, the mean Pdct decreased by 1 +/- 2 cm H2O (NS) and the mean compliance increased by 1 +/- 2 ml/cm H2O (NS) in the post-normal saline study. These results show that TRH may improve bladder function in patients with injury-induced spinal shock by increasing detrusor pressure and by decreasing bladder compliance.
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PMID:Modulation of urinary bladder function with thyrotropin-releasing hormone in patients with spinal cord injuries during the spinal shock phase. 641 Sep 71

Cold intolerance and secondary amenorrhea developed in a patient who had meningoencephalitis 4 yr prior to study. A clinical diagnosis of hypothalamic hypothyroidism was made on the basis of low serum thyroxine and triiodothyronine levels, and low plasma thyrotropin concentrations, which were responsive to thyrotropin-releasing hormone (TRH). The secretion of the remaining pituitary hormones (growth hormone, prolactin, adrenocorticotropin and gonadotropins) was intact. Not only was thyroid function normalized by oral administration of TRH, but also menses resumed after adequate replacement therapy with thyroid hormone. These results imply that hypothyroidism in this patient was due to isolated dysfunction of hypothalamic TRH release.
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PMID:Hypothalamic hypothyroidism due to isolated thyrotropin-releasing hormone (TRH) deficiency. 643 93


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