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)

A pharmacologic approach was used to examine the possible role of dopamine neurons in the regulation of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) secretion in the rat. Blockade of dopamine receptors by haloperidol or pimozide treatment evoked dose- and time-related increases in plasma levels of beta-END-LI. Physical immobilization increased circulating beta-END-LI six-fold and pretreatment with dopamine receptor agonists (bromocriptine or pergolide) significantly attenuated this rise without affecting plasma beta-END-LI levels in non-stressed animals. Dopaminergic drugs and immobilization produced similar effects on circulating PRL as on beta-END-LI. However, the magnitude of change in levels of PRL was generally greater than the change in beta-END-LI. The present findings suggest that dopaminergic neurons inhibit the release of pituitary beta-END-LI as well as PRL in the rat.
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PMID:Dopaminergic inhibition of pituitary beta-endorphin-like immunoreactivity secretion in the rat. 627 43

Several tetrahydroisoquinolines (TIQs) were tested for their in vitro and in vivo capacities to modulate prolactin (PRl) and beta-endorphin (beta-end) secretion by the rat pituitary and for their abilities to displace [3H]spiroperidol and [3H]naloxone binding from pituitary and hypothalamic membranes. Receptor binding studies showed that TIQs could be classified as having (a) higher affinity for opiate receptors (tetrahydropapaverine, papaverine, 6-methylsalolinol, 1-carboxysalsolinol and 3',4'-deoxy-norlaudanosolinecarboxylic acid), (b) higher affinity for the dopamine receptor (salsolinol and 7-methylsalsolinol), or (c) approximately equal affinity for the two binding sites (6,7-dimethylsalsolinol and tetrahydropapaveroline, THP). In freely moving male rats, THP produced a several-fold increase in plasma PRL levels. This effect was not altered by co-administration of naloxone but was attenuated by dopamine. In vitro several TIQs reversed the inhibitory effect of dopamine on PRL secretion by cultured anterior pituitary cells. The order of potencies of the TIQs in this system paralleled their order of potencies in the dopamine receptor assay. THP, the most potent dopamine antagonist, also blocked dopamine-mediated inhibition of beta-endorphin secretion from neurointermediate lobe cells in culture. These data demonstrate that THP and some other TIQs can act as dopamine antagonists in radioreceptor assays, in cell culture and in vivo.
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PMID:In vivo and in vitro effects of tetrahydroisoquinolines and other alkaloids on rat pituitary function. 628 72

A pituitary tumor from a patient with severe Cushing's disease and marked hyperprolactinemia was extensively studied by immunohistochemical techniques. Tissues from two separate areas of the adenoma were found to contain similar cell proportions of PRL as well as ACTH and related peptides (beta-lipotropin, beta-endorphin, and alpha MSH). The tumor was composed of approximately 70% immunoreactive PRL cells and 5% ACTH-containing cells. Double immunostaining revealed that PRL or ACTH and related peptides were found in two distinct populations of tumor cells. These results document for the first time inappropriate synthesis and secretion of an unusual combination of pituitary hormones from a mixed pituitary adenoma.
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PMID:Concurrent production of adrenocorticotropin and prolactin from two distinct cell lines in a single pituitary adenoma: a detailed immunohistochemical analysis. 628 57

Thirteen pituitary adenomas were removed from patients with Cushing's disease by the transphenoidal route. All cases demonstrated a typical histochemical and ultrastructural pattern. Immunocytochemical study by means of the immunoperoxidase technique and light or electron microscopy demonstrated 1-24/1-39 adrenocorticotropic hormone (ACTH) in all cases, lipotropin/melanotropin (beta-LPH/beta-MSH) in 10 cases, beta-endorphin in 8 cases, and an absence of calcitonin in all cases. In addition, in 2 cases tumor tissue contained a few antiprolactin immunoreactive cells. These ACTH, beta-LPH, and beta-endorphin immunoreactivities may reflect either the peptides themselves or their precursors or intermediate products. The authors also suggest a possible intermediate-lobe-like processing of beta-LPH leading to beta-endorphin production, which may act on PRL cells. In addition, no positive arguments for the existence of a common precursor for calcitonin and ACTH could be provided from this study.
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PMID:Immunohistochemical and immunoelectron-microscopic study of pituitary adenomas associated with Cushing's disease. A report of 13 cases. 628 70

Several peptides normally produced in the anterior pituitary lobe were searched in rat antral mucosa by immunocytochemistry. Peptides derived from pro-opiomelanocortin were tested: some endocrine cells were immunoreactive with ACTH 17-39 antiserum, and only a few elements were stained with ACTH 1-24 and beta LPH antisera. No immunoreactive cells were observed using alpha MSH, beta MSH and beta endorphine antisera. Using an antiserum against beta endorphin, a few cells and nerve fibres were immunostained. The other pituitary hormones were also tested: numerous antral cells contained immunoreactive GH, and some cells immunoreactive PRL or compounds chemically related to these hormones. No cells were stained with antisera directed against glycoproteic hormones. This work showed that several peptides previously localized in the pituitary gland were found in the antral mucosa. Further studies are needed to identify the cell types containing these peptides and to determine their origin.
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PMID:[Immunohistochemical localization of pituitary peptides in the rat pyloric antrum mucosa]. 629 30

The 41-residue ovine corticotropin releasing factor (CRF) was administered iv and intracerebroventricularly (icv) to merino sheep. A significant rise in plasma ACTH, beta-lipotropin (beta LPH) and cortisol was demonstrated after the administration of 200 micrograms, iv. A highly significant correlation between the increments in plasma ACTH and beta LPH was observed. The plasma ACTH rise was evident within 5 min and was abolished by the prior administration of 0.4-4.0 mg dexamethasone. No significant rise in plasma GH, LH, PRL, insulin, glucagon, pancreatic polypeptide, met-enkephalin, angiotensin II, aldosterone, or vasopressin could be demonstrated. Although smaller doses of CRF (50 ng to 5 micrograms) were effective when given icv, the ACTH response was more delayed. It is concluded that CRF stimulates a rapid increase in the secretion of ACTH and beta LPH in sheep. Suppression of this response by dexamethasone indicates that glucocorticoids are capable of acting on the pituitary to inhibit the ACTH response to CRF. The delayed response when CRF is given icv may be due to diffusion. The action of CRF appears to be relatively specific, in that the plasma concentrations of the other pancreatic, pituitary, and adrenal hormones measured were not affected.
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PMID:The hormonal actions of corticotropin-releasing factor in sheep: effect of intravenous and intracerebroventricular injection. 630 69

To determine the effect of beta-endorphin on the pituitary-adrenal axis, human synthetic beta-endorphin was infused iv in 10 normal human subjects. Either beta-endorphin (0.3, 1.0, and 3.0 micrograms/kg . min, each dose for 30 min) or a control (sham) infusion of 5% dextrose water was administered in a blind fashion in the same subjects on 2 successive days. Plasma ACTH and cortisol and serum human GH and PRL levels were measured 30 min before and then every 30 min for 210 min during and after both the beta-endorphin and control infusions. In all subjects, cortisol levels decreased below the basal level in response to the infusion of beta-endorphin. The threshold dose was 1.0 micrograms/kg . min, with the mean control cortisol level (12 +/- 2 micrograms/dl) declining significantly to 7 +/- 1 micrograms/dl (1.0 micrograms/kg . min) and 6 +/- 1 micrograms/dl (3.0 micrograms/kg . min; P less than 0.01). ACTH levels also were significantly lower than the control value (48 +/- 6 pg/ml) at the 1.0 microgram/kg . min dose (32 +/- 4 pg/ml; P less than 0.05). The decline in ACTH and cortisol levels was also significantly different from levels obtained during the control infusions (P = 0.001 and P = 0.01, respectively). The results are consistent with short feedback loop inhibition of pituitary ACTH release or suppression of hypothalamic corticotropin-releasing factor release by beta-endorphin.
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PMID:beta-endorphin suppresses adrenocorticotropin and cortisol levels in normal human subjects. 630 33

In postmenopausal women, the administration of beta-endorphin in repeated pulses (1-2.5 mg) at 1- to 2-h intervals or constant infusion (1 mg/h) for 3-6 h elicited the prompt release of PRL without concomitant change in LH levels. Infusion of an opiate receptor antagonist, naloxone (1.6 mg/h), for 6-7 h also had no effect on LH levels. Since substantial evidence indicates that endogneous opioid peptides exert an inhibitory role on GnRH-LH secretion and that the functional activity of opiate receptors appears to be ovarian steroid dependent, the present observation suggests that the hypersecretion of gonadotropin in the absence of ovarian steroid feedback may, in part, be causally related to a reduced opioid inhibition of GnRH-LH release.
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PMID:The disappearance of opioidergic regulation of gonadotropin secretion in postmenopausal women. 631 28

We have investigated the influence of endogenous opiates on hormone responses during suckling in the rat. In complementary experiments, opiate receptors were blocked by naloxone (NAL) or endogenous opiate release from the pituitary was inhibited by dexamethasone (DEX). Serial blood samples from unanesthetized suckled rats were then assayed for plasma PRL, beta-endorphin-like immunoreactivity (beta-END-LI), TSH, and GH levels. Identical studies were also done in saline-treated (control) suckled rats and in unsuckled rats exposed to control objects. Whereas suckling caused a rise in plasma PRL, beta-END-LI, and GH, introduction of plastic control objects did not elevate hormone levels. NAL blocked the GH rise and depressed TSH levels, but did not significantly inhibit the PRL or beta-END-LI response. DEX prevented the beta-END-LI rise and blocked the GH rise, but did not inhibit TSH. DEX enhanced PRL release during suckling. These results demonstrate that 1) the responses of beta-END-LI, PRL, and GH are not an artifact of the sampling procedure; 2) PRL release during suckling is independent of beta-END-LI release by the pituitary; and 3) suckling stimulates the release of ACTH, beta-END, and beta-lipotropin from the anterior pituitary. Our results are consistent with both a role of pituitary beta-END in the control of GH and a role of corticosterone in the control of PRL during suckling.
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PMID:Opiate modulation of the anterior pituitary hormone response during suckling in the rat. 632 36

The fetal porcine pituitary was investigated by means of ultrastructural immunocytochemistry (1) to identify the first cells synthesizing the adenohypophyseal hormones, (2) to follow their differentiation during fetal development, and (3) to compare their ultrastructural characteristics with those of mature adult cells. The first ACTH-cells, which produced and stored ACTH, beta-LPH, beta-MSH, and alpha- and beta-endorphin in the same granules, were very numerous at day 34 and displayed a uniform morphology. At day 50 and thereafter, until the end of gestation, the ACTH-cells differed in their appearance probably reflecting various stages of differentiation of one cell type. The GH-cells gained rapidly ultrastructural features comparable to those of mature GH-cells. In contrast, in the case of PRL-cells, which appeared only at the end of the gestation period as immature elements containing very small secretory granules, the morphological maturation seemed to take place only after birth. The first cells synthesizing the glycoprotein hormones (LH alpha, LH beta, FSH and TSH) displayed ultrastructural features of immature cells. At day 50, their ultrastructural organization started to show a different pattern. At the end of gestation, the TSH-cells and the gonadotropic cells displayed the ultrastructural features of mature cells.
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PMID:Functional differentiation of the anterior pituitary cells in the fetal pig. An ultrastructural immunocytochemical study. 632 16


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