Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using autoradiography combined with immunocytochemistry, we demonstrated that the target cells of CRH in the human pituitary were proopiomelanocortin cells. Scatchard analysis of [125I]Tyr0-oCRH saturation binding revealed the presence of one class of saturable, high affinity sites on pituitary tissue homogenate. The equilibrium dissociation constant (Kd) for [125I]Tyr0-oCRH ranged from 1.1-1.6 nM, and the receptor density was between 200-350 fmol/mg protein. Fixation of cryostat sections with 4% paraformaldehyde before tracer incubation improved both tissue preservation and localization of the CRH receptor at the cellular level. Additional postfixation with 1% glutaraldehyde inhibited tracer diffusion during subsequent immunocytochemistry and autoradiography. [125I]Tyr0-oCRH was found in cytoplasmic inclusions or at the cell periphery of ACTH/beta-endorphin cells in the anterior pituitary. Single cells of the posterior pituitary were also CRH receptor positive. Cells staining for PRL or GH were CRH receptor negative. We conclude that CRH binds only to high affinity receptors on ACTH/beta-endorphin cells in the human pituitary.
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PMID:Receptors for corticotropin-releasing hormone in human pituitary: binding characteristics and autoradiographic localization to immunocytochemically defined proopiomelanocortin cells. 164 37

Bilateral, selective, and simultaneous catheterization of the inferior petrosal sinus is not only a valuable tool in the differential diagnosis of Cushing's syndrome, but may also provide new insights into paracrine interactions at the pituitary level. We have investigated whether CRH (1 microgram/kg BW) has any effect on the release of PRL, GH, TSH, or the alpha-subunit of hCG during this procedure. Sixteen patients under evaluation for Cushing's syndrome (Cushing's disease, n = 12; ectopic ACTH syndrome, n = 2; glucocorticoid resistance, n = 1; hormonally inactive adenoma, n = 1) were catheterized. Two of the patients with Cushing's disease received 4.0 mg naloxone iv 15 min before stimulation with CRH. Patients with Cushing's disease demonstrated a central/peripheral gradient and an intersinus gradient not only for ACTH, but also for PRL, alpha-subunit, GH, and TSH, provided that the latter two hormones were not completely suppressed by the glucocorticoid excess. Moreover, all hormones increased in response to CRH on the side with the highest ACTH concentration; PRL rose from 31.2 +/- 6.4 to 61.6 +/- 12.4 micrograms/L (P less than 0.01), and alpha-subunit from 2.6 +/- 0.6 to 6.4 +/- 1.7 micrograms/L, (P less than 0.01). Naloxone was unable to abolish the PRL or alpha-subunit increase in response to CRH. A multihormonal response to CRH in inferior petrosal sinus blood was also observed in the patient with glucocorticoid resistance and in the patient with the hormonally inactive tumor, but not in the patients with ectopic ACTH secretion. The multihormonal response to CRH could be explained by cosecretion of other hormones together with ACTH from corticotroph adenoma, by an effect of CRH on pituitary blood flow, or by a paracrine action of pituitary corticotrophs on adjacent normal pituitary cells. Our results do not support the concept that such a paracrine action is mediated by beta-endorphin. However, a higher dose of naloxone may be required to antagonize the action of pituitary beta-endorphin.
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PMID:A multihormonal response to corticotropin-releasing hormone in inferior petrosal sinus blood of patients with Cushing's disease. 169 62

The effects of chronic administration of met-enkephalin (40 micrograms/day, for 20 days) on the pituitary prolactin cells of Wistar male rats were studied at the light (PAP-immunohistochemical for PRL demonstration technique) and electron microscopy levels. The D. CIRCLE (mean diameter), D. MAX (maximum diameter) and FORM PE (circular factor of form; irregularity degree) form secretory granules, as well as their percent distribution, were also evaluated. The cellular alterations were variable. Most prolactin cells showed an increase in immunohistochemical reaction. At the electron microscope level the prolactin cells showed an enlargement and swelling of the RER and Golgi apparatus. The secretory granules were bigger and more spherical in experimental than in untreated and control animals. A number of cells showed a variable number of cytoplasmic vacuoles or a large central vacuole formed from dilated RER-cisternae. The authors discuss the possible mechanism whereby met-enkephalin exerts a control on prolactin cells.
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PMID:Ultrastructural, immunocytochemical and morphometric studies of pituitary prolactin cells after chronic administration of met-enkephalin. 179 Mar 47

Intravenous interleukin-2 (IL-2) administration has been shown to influence several hormonal secretions. The present study was carried out to investigate the endocrine effects of subcutaneous therapy with IL-2. Six patients with advanced renal cancer were studied. They were treated subcutaneously with IL-2 according to the schedule proposed by Atzpodien et al. Venous blood samples were collected at O-time and 1, 8 and 12 hours after the first IL-2 pulse of 9 X 10(6) IU/m2 at 8.00 a.m.; on a separate occasion, samples were collected during a saline infusion only. In each blood sample, serum levels of cortisol, beta-endorphin, GH, PRL, FSH, LH, TSH and the pineal hormone melatonin were measured by RIA. Both cortisol and beta-endorphin significantly increased after IL-2 injection. GH rose but not to a significant extent. PRL, FSH, LH and TSH did not change after IL-2. Finally, melatonin levels markedly decreased after IL-2 injection in the only 2 patients with elevated concentrations of this hormone before the start of immunotherapy. These results suggest that the endocrine effects of subcutaneous IL-2 therapy are similar to those previously described with intravenous administration.
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PMID:Neuroendocrine effects of subcutaneous interleukin-2 injection in cancer patients. 186 47

The neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
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PMID:The role of histamine in the neuroendocrine regulation of pituitary hormone secretion. 206 91

Several experiments have demonstrated that there is a relationship between neuroendocrine and immune systems. Despite these interesting findings, only few studies have been performed up to now to evaluate the possible importance of neuroimmune interactions in influencing the biological efficacy and toxicity of cancer immunotherapy with IL-2. To analyze the effects of IL-2 on endocrine secretions, we have measured by RIA serum levels of cortisol, beta-endorphin, GH, PRL and of the pineal hormone melatonin in metastatic renal cancer patients, treated with 5-day courses of IL-2 at a daily dose of 3 x 10(6) U/m2, given through a 24-hour intravenous infusion. Six IL-2 courses were evaluated, by collecting blood samples at 4-hour intervals for 24 hours and by comparing the hormonal values with those observed in baseline conditions. Both cortisol and beta-endorphin mean values significantly increased during IL-2 infusion. GH and PRL also increased, but not in a significant manner. Finally, melatonin mean levels significantly decreased during the infusion. The IL-2-induced effects on cortisol, beta-endorphin and melatonin resulted in a complete abolition of their physiological circadian rhythm. These results show that IL-2 infusion induces important changes in endocrine secretions. Because of the immunosuppressive effect of cortisol and the stimulatory one of melatonin, their changes during IL-2 infusion might influence the biological activity of immunotherapy itself. Further studies will be required to define better the clinical importance of IL-2 induced hormonal changes.
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PMID:Endocrine effects of a 24-hour intravenous infusion of interleukin-2 in the immunotherapy of cancer. 214 95

The ability of alpha MSH, a POMC-derived peptide, to antagonize the effects of beta-endorphin (beta EP) on PRL and LH secretion was studied in the primate. Seven ovariectomized rhesus monkeys bearing chronic indwelling third ventricular catheters for peptide infusion were used for these studies. Peripheral blood samples for PRL and LH RIA were obtained every 15 min during a 3-h control period when saline was infused into the ventricle, followed by a 5-h period of peptide infusion at a rate of 25 microliters/h. When beta EP was infused at a dose of 5 micrograms/h, plasma PRL rose from a mean baseline of 3.5 +/- 0.7 ng/ml to a peak of 21.3 +/- 2.2 ng/ml. When the same animals were infused with 20 micrograms alpha MSH together with 5 micrograms beta EP, the peak concentration of PRL was reduced to 8.2 +/- 1.7 ng/ml (P less than 0.001). When a higher dose of beta EP (20 micrograms/h) was infused, PRL rose to a peak of 38.2 +/- 1.8 ng/ml. This response was again markedly blunted, and the peak PRL response was reduced to 7.3 +/- 2.2 ng/ml when 20 micrograms beta EP were infused together with 80 micrograms alpha MSH (P less than 0.001). Analysis of the area under the plasma PRL concentration curves demonstrated a significant reduction in area during the 5-h infusion with beta EP plus alpha MSH compared to that during infusion of beta EP alone. The mean area was reduced from 3480 +/- 570 ng min/ml after 5 micrograms beta EP alone to 1030 +/- 200 after 5 micrograms beta EP plus 20 micrograms alpha MSH and from 6230 +/- 990 after 20 micrograms beta EP to 1020 +/- 320 ng min/ml after 20 micrograms beta EP plus 80 micrograms alpha MSH (P less than 0.01). Des-acetyl alpha MSH (80 micrograms) was also effective in reducing the PRL response to 830 +/- 380 ng min/ml (P less than 0.05). The suppression of pulsatile LH release by beta EP was also attenuated by alpha MSH. During the 5-h infusion of beta EP, total LH secretion was reduced to 65.9 +/- 3.8% of that measured during the 3-h saline infusion compared to 87.2 +/- 2.7% after infusion of beta EP plus alpha MSH (P less than 0.001) or 91.7 +/- 4.1% after beta EP plus des-acetyl alpha MSH (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interaction between beta-endorphin and alpha-melanocyte-stimulating hormone in the control of prolactin and luteinizing hormone secretion in the primate. 215 79

A 44-yr-old man with hypocortisolism was shown to have an undetectable basal plasma ACTH level and absent or subnormal ACTH and beta-lipotropin responses to provocative testing with insulin, vasopressin, and CRH. Endocrine function after glucocorticoid replacement was otherwise normal, thus establishing the diagnosis of isolated ACTH deficiency. This patient's serum was tested immunohistochemically for the presence of an antipituitary antibody by indirect immunofluorescence of rat pituitary tissue. Positive immunostaining was observed in stellate-shaped cells in the anterior and intermediate lobes. Immunopositive cells were shown by immunoelectron microscopy to have ultrastructural characteristics of corticotrophs. Immunoreactivity was concentrated in secretory granules 120-170 nm in diameter. In a double immunolabeling procedure, staining by the patient's serum was shown to colocalize with rabbit antiserum to ACTH, but not with antisera to PRL, GH, beta TSH, or beta LH. Immunoabsorption of the patient's serum with ACTH-(1-24), ACTH-(1-39), gamma MSH, corticotropin-like intermediate lobe peptide, beta-endorphin, or beta-lipotropin failed to diminish immunolabeling in the pituitary. We conclude that the antipituitary antibody in this patient's serum shows immunohistochemical specificity for a rat corticotroph antigen located in secretory granules that is neither ACTH nor any of the proopiomelanocortin (POMC)-derived peptides tested. The autoantigen could be a cell-specific granular factor involved in the posttranslational processing of POMC or secretion of ACTH. We postulate that an autoimmune process may account for this patient's disease, and that his antipituitary antibody could play a pathogenic role by either inhibiting a POMC-processing enzyme or initiating an antibody-dependent cell-mediated cytotoxicity reaction, resulting in the selective destruction of corticotrophs.
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PMID:Isolated adrenocorticotropin deficiency associated with an autoantibody to a corticotroph antigen that is not adrenocorticotropin or other proopiomelanocortin-derived peptides. 215 84

Although the role of serotonin (5HT) in the regulation of anterior pituitary hormone secretion is well documented, the involvement of specific 5HT receptor subtypes in this action is not yet fully elucidated. In the present work we attempted to determine the neuroendocrine role of the 5HT1A receptor subtype. This was chosen mainly because highly selective pharmacological tools are available for that subtype. 8-Hydroxy-2-(di-n-propylamino)tetralin (8OHDPAT) and ipsapirone were injected iv in conscious, freely moving male rats cannulated in the jugular vein. For the sake of comparison, a 5HT receptor agonist with preference for the 5HT1B and 5HT1C receptor subtypes 1-(m-trifluoromethyl-phenyl)piperazine (TFMPP) was also administered. Plasma PRL, ACTH, and beta-endorphin levels increased in a dose-dependent manner after 8-OHDPAT (0.01-1 mg/kg) or ipsapirone (0.5-7.5 mg/kg) injection. Maximal effects were obtained between 7-15 min. Only the highest dose of 1-(m-trifluoromethyl-phenyl)piperazine (5 mg/kg) resulted in the same response. In contrast, none of the drugs used affected plasma GH, TSH, or LH levels at any dose tested. The results indicate that 5HT1A receptors are involved in the regulation of PRL as well as ACTH and beta-endorphin secretion. 8OHDPAT was almost 40 times more potent than ipsapirone. The maximal effects of the two drugs on PRL release were comparable. In contrast, ipsapirone behaved as a partial agonist only on ACTH and beta-endorphin secretion, thus suggesting that different neuronal targets are involved in the stimulation of the three hormones by 5HT.
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PMID:Changes in anterior pituitary hormone levels after serotonin 1A receptor stimulation. 216 13

To evaluate the nature of anterior pituitary secretory events in vivo, we have applied a novel waveform-independent deconvolution technique that dissects the underlying secretory behavior of endocrine glands quantitatively from available serial plasma hormone concentration measurements assuming one- or two-compartment elimination kinetics. We used this new tool to ask the following physiological questions. 1) Does the pituitary gland secrete exclusively in randomly dispersed bursts, and/or does a tonic (constitutive) mode of interburst hormone secretion exist? 2) What secretory mechanisms generate the nyctohemeral rhythms in plasma hormone concentrations? Analysis of 24-h plasma concentration profiles of GH, LH, FSH, PRL, TSH, ACTH, and beta-endorphin (n = 6-8 men/group) revealed that 1) pituitary secretion in vivo occurs in an exclusively burst-like mode for all hormones except TSH and PRL (for the latter two, a mixed burst and constitutive mode pertained); 2) significant nyctohemeral regulation of secretory burst frequency alone was not demonstrated for any hormone; 3) prominent 24-h variations in secretory burst amplitude alone were delineated for ACTH and LH; 4) TSH, GH, and beta-endorphin were both frequency and amplitude controlled; 5) no significant diurnal variations in FSH secretory parameters occurred; and 6) a fixed hormone half-life yielded fits of the 24-h data series with a normalized residual variance of less than 8%. We conclude that the normal human anterior pituitary gland releases its multiple (glyco)protein hormones via punctuated secretory episodes unassociated with tonic basal (constitutive) hormone secretion, except in the case of TSH and PRL. Hormone-specific amplitude and/or frequency control of secretory burst activity over 24 h provides the mechanistic basis for the classically recognized 24-h rhythms in plasma concentrations of adenohypophyseal hormones in men.
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PMID:Twenty-four-hour rhythms in plasma concentrations of adenohypophyseal hormones are generated by distinct amplitude and/or frequency modulation of underlying pituitary secretory bursts. 217 82


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