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)

Effects of growth hormone-releasing hormone (GRH) and corticotropin-releasing hormone (CRH) on the release of immunoreactive thyrotropin-releasing hormone (ir-TRH) from the rat hypothalamus in vitro were studied. The rat hypothalamus was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) for 20 min. The amount of ir-TRH release into the medium was measured by radioimmunoassay. The ir-TRH release from the rat hypothalamus was inhibited significantly in a dose-related manner with the addition of GRH or CRH. These findings suggest that GRH and CRH inhibit ir-TRH release from the rat hypothalamus in vitro.
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PMID:Effects of growth hormone-releasing hormone and corticotropin-releasing hormone on the release of thyrotropin-releasing hormone from the rat hypothalamus in vitro. 313 Nov 50

Intracerebroventricular administration of TRH induces excessive grooming behavior that is characterized by an important contribution of the elements scratching and paw licking. As compared with other grooming inducing peptides, the pattern of TRH-induced grooming resembles that induced by beta-endorphin rather than those elicited by ACTH or bombesin. TRH-induced excessive grooming is suppressed by pretreatment with haloperidol, naloxone or neurotensin. Haloperidol suppresses TRH-induced grooming in a general way, whereas the suppressive effect of the other drugs is mainly due to a selective reduction of TRH-induced excessive scratching. Combined treatments of rats with TRH and a submaximal dose of ACTH, bombesin or beta-endorphin do not result in higher grooming scores than with single peptide treatment. Excessive grooming elicited by water immersion is not affected by TRH. It is concluded that TRH is undoubtedly an excessive grooming inducing peptide. In situations where excessive grooming is elicited by other peptides or by water immersion, TRH does not further activate the operating systems involved in the existing excessive grooming.
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PMID:Some characteristics of TRH-induced grooming behavior in rats. 313 46

The effect of modifications of extracellular calcium concentrations on alpha-MSH release has been studied using perifused frog neurointermediate lobes. Increasing concentrations of calcium (from 2 to 10 mmol/l) gave rise to a dose-related stimulation of alpha-MSH secretion, whereas reduction of Ca2+ from 2 to 1.5 mmol/l partially inhibited alpha-MSH release. The direct effect of extracellular Ca2+ on alpha-MSH secretion was confirmed by the dose-dependent stimulation of alpha-MSH release induced by the calcium ionophore A23187. Perifusion with a calcium-free medium or blockade of Ca2+ channels by 4 mmol Co2+/l both resulted in an inhibition of spontaneous and TRH-induced alpha-MSH release. Conversely, administration of verapamil or methoxyverapamil (10 mumol/l each) did not alter basal secretion and had no effect on the response of the glands to TRH. Nifedipine (10 mumol/l), which was able to block KCl (20 mmol/l)-evoked alpha-MSH release, induced a slight inhibition of basal alpha-MSH secretion, indicating that extracellular Ca2+ levels may regulate alpha-MSH release in part by Ca2+ influx through voltage-dependent Ca2+ channels. In contrast TRH-induced alpha-MSH release was not affected by nifedipine or dantrolene (10 mumol/l), and BAY-K-8644 (1 mumol/l) did not significantly modify the response of neurointermediate lobes to TRH. Taken together, these results suggest that TRH-induced alpha-MSH secretion is associated with calcium influx across the plasma membrane and that calcium entry caused by TRH may occur through nifedipine/verapamil-insensitive Ca2+ channels.
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PMID:Role of calcium in thyrotrophin-releasing hormone-stimulated release of melanocyte-stimulating hormone from frog neurointermediate lobe. 315 Dec 49

The observation that suckling evokes a modest rise in serum TSH when compared with that of prolactin is inconsistent with the hypothesis that TRH serves as a hypophysiotropic mediator of this response. In the present study we attempted to provide an explanation for this discrepancy by determining whether any of a growing number of putative prolactin releasing factors could alter pituitary responsiveness to TRH. Anterior pituitaries from lactating (day 14) rats were monodispersed with trypsin, cultured for 2 days, and then incubated in the presence of medium alone or medium containing TRH, dopamine, or a combination of these secretagogues. Companion sets of cultures were incubated concurrently with either beta-endorphin, neurotensin, oxytocin, serotonin, vasoactive intestinal polypeptide, or lysine vasopressin. As expected, TRH stimulated and dopamine suppressed prolactin release. None of the substances tested except oxytocin had a significant effect on pituitary cell responsiveness to TRH or dopamine. Oxytocin had no effect on prolactin secretion when tested alone or in combination with TRH and dopamine. TRH alone stimulated TSH release by these cultures, while oxytocin and dopamine were ineffective by themselves. However, TSH secretion by cultures treated simultaneously with TRH and oxytocin could be suppressed to approximately half of that released by cells incubated with TRH alone. These results demonstrate that oxytocin attenuates TRH-induced TSH release by a direct action on pituitary cells without affecting the prolactin response. This selectivity of responsiveness imparted by oxytocin might contribute to the blunted release of TSH after suckling.
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PMID:Oxytocin attenuates TRH-induced TSH release from rat pituitary cells. 315 75

Male golden hamsters were exposed to long photoperiod or short photoperiod (SP) and injected with 1 microgram TRH and/or 1 microgram LHRH at lights on (LO) or lights off (LX) for a total of 8 weeks. Both TRH and LHRH prevented testicular regression if they were injected at LO. Injected at LX, TRH did not prevent testicular regression, and LHRH was only partially effective. Plasma beta-endorphin levels were significantly higher in groups with atrophic testes. These results indicate that TRH like LHRH can prevent SP-induced testicular regression in hamsters by some unknown mechanism and that beta-endorphin may be involved in the control of testicular function in hamsters.
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PMID:Temporal difference of thyrotropin-releasing hormone in prevention of testicular regression in golden hamsters exposed to short photoperiods: possible involvement of beta-endorphin. 315 80

The present study records the physiological effects of 24-hour intracerebroventricular infusion of a variety of biologically active peptides in conscious sheep. A number of peptides including AVP and TRH produced increases in mean arterial pressure, heart rate and body temperature. There was an overall positive correlation between peptide-induced changes in body temperature and changes in either mean arterial pressure or heart rate. TRH and beta-endorphin had marked effects on behaviour and several peptides reduced food and water intake. Several peptides increased urinary sodium excretion, however, few peptides changes plasma electrolyte concentrations. TRH produced small effects on plasma ACTH and plasma glucose concentrations. The peptides in this study produced physiological changes which were probably mediated by their actions on the central nervous system.
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PMID:The effects of intracerebroventricular administration of biologically active peptides in conscious sheep. 324 47

The time course of hormone concentrations in response to a stimulus can be characterized with kinetic methods to express rates of hormone release and elimination, total amount of hormone release and expected best times for blood sampling. Routine application of kinetic methods should increase the sensitivity and applicability of hormonal challenge tests. Applications to the TRH test and to prolactin release measurements are reviewed. A new kinetic model for continuously collected samples is applied to measurements of met-enkephalin release in rats. Calculations indicated an initial concentration of 1876 pg/ml and a ventricular volume of distribution of 0.25 ml. After exposure of rats to nitrous oxide, the rate of release of met-enkephalin-like activity into the ventricles rose from 3.4 to 8.3 pg/min.
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PMID:Kinetic modeling of hormone release: application to time-averaged met-enkephalin release. 343

The cells of the frog pars intermedia synthesize a 36 000 (36K) protein called proopiomelanocortin (POMC). After [3H]glucosamine incorporation, separation of newly synthesized products by SDS-polyacrylamide gel electrophoresis showed that this 36K protein was glycosylated. Tryptic mapping revealed only one site of glycosylation and showed that the carbohydrate side-chain was located in the N-terminal region of POMC. The 36K protein was not released by the melanotrophs, but it generated, through specific intracellular proteolytic cleavage, a number of smaller peptides which were subsequently released. These peptides were identified by various methods including selective amino-acid incorporation, HPLC purification, acid-urea gel electrophoresis, tryptic and chymotryptic mapping, assay of melanotropic activity, radioimmunoassays and immunoprecipitations. Some of the newly synthesized N-terminal (18K) fragment of the POMC was secreted intact while a portion of it was further processed, via an intermediate peptide, to give mature gamma-MSH. All three of these peptides were glycosylated. In addition, the mature peptide (gamma-MSH) exhibited a low but significant melanotropic activity. The C-terminal portion of the prohormone was very rapidly processed to give des N alpha-acetyl alpha-MSH, corticotropin-like-intermediate lobe peptide (CLIP) and beta-endorphin. Authentic alpha-MSH was always absent in cellular extracts: acetylation to give rise to alpha-MSH was a late enzymatic process strictly linked to hormonal release. Since acetylation of alpha-MSH is required for full biological activity of this peptide, it is possible to conceive that this later step could be under neuroendocrine control. Using the perifusion technique we have been able to show the complexity of the control mechanisms regulating amphibian melanotrophs. It is generally accepted that the aminergic innervation of the intermediate lobe of the pituitary is involved in the hypothalamic control of melanotropin release. We have demonstrated that, in amphibians, dopamine inhibits alpha-MSH secretion through D2-type dopaminergic receptors whereas norepinephrine and (or) epinephrine stimulate alpha-MSH secretion via beta-adrenergic receptors. The existence of peptidergic fibers within parenchymal cells of the pars intermedia has been demonstrated. Evidence for TRH-containing fibers has been obtained by immunohistochemistry. Using a specific radioimmunoassay for TRH, we have confirmed the presence of TRH in the neurointermediate lobe of the frog. We have shown that TRH is a powerful MSH-releasing factor in these animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Intermediate lobe of the amphibian pituitary gland: an endocrine gland with multiple secretions and under multi-hormonal control]. 392 69

A 33-year-old male was admitted to the Department of Neurosurgery, Fukui Medical School with a complaint of headache. There were no neurological deficits on admission. Craniogram demonstrated a so-called "phantom sella". A computed tomography revealed a high density mass lesion and the mass was enhanced well, that mainly extended from the sella to the left middle cranial fossa. The left carotid angiogram revealed an avascular mass lesion extending from the sella to the left middle cranial fossa. Pituitary function tests revealed an extremely high serum prolactin (PRL) levels (70, 100 ng/ml). PRL response to TRH was delayed in peak and the high level continued. Serum PRL levels elevated to 90, 800 ng/ml at 180 min after injection of TRH. A biphasic response was demonstrated in response to CB-154 suppression test to PRL secretion, that is, CB-154 stimulated PRL release initially (up to 90 min) and suppressed thereafter. Serum PRL levels (178, 400 ng/ml) reached to peak about 90 min after CB-154 administration. Response of growth hormone (GH) and adrenocorticotropic hormone (ACTH) to insulin were also impaired. Craniotomy was performed. The tumor was partially removed and was diagnosed as a prolactinoma histologically. Tumor tissue removed was subjected to the monolayer culture and electron microscopic study. Their observations demonstrated hyperactive PRL secretion of the individual cells. A total dose of 5,000 rads was irradiated postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of male prolactinoma presenting extremely high serum prolactin levels and biphasic response to CB-154 suppression test]. 404 Dec 91

An assay for the binding of [(3)H]thyrotropin-releasing hormone ([(3)H]TRH) is described. Plasma membranes isolated from bovine anterior pituitary gland bind about 600 femtomoles of this hormone per mg of protein, as compared to 15 femtomoles per mg of protein in the total adenohypophyseal homogenate (40-fold purification). The equilibrium constant of membrane receptor-[(3)H]TRH binding at 0 degrees C is 4.3 x 10(7) L.M(-1), or a half-maximal binding of this hormone at 23 nM. The binding is time-dependent; addition of unlabeled hormone induces dissociation of the receptor-[(3)H]TRH complex with a half-life of 14 min. The binding of TRH is not altered by 10 muM melanocyte-stimulating hormone-release inhibiting hormone, lysine-vasopressin, adrenocorticotropin, growth hormone, prolactin, luteinizing hormone, insulin, glucagon, L-thyroxine, or L-triiodothyronine. K(+) and Mg(++) increase formation of the receptor-TRH complex at optimal concentrations of 5-25 mM and 0.5-2.5 mM, respectively, with inhibition at higher concentrations. Ca(++) inhibits binding of TRH at all concentrations tested.
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PMID:Binding of thyrotropin-releasing hormone to plasma membranes of bovine anterior pituitary gland (hormone receptor-adenylate cyclase-equilibrium constant-( 3 H)thyrotropin). 462 48


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