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)

Normal subjects were studied to test the feasibility of a combined anterior pituitary function test using iv administration of four hypothalamic releasing hormones: ovine corticotropin-releasing hormone, human GH-releasing hormone, GnRH, and TRH. Initially, nine normal men were studied with various combinations of these four hormones to exclude the possibility that they might inhibit or synergize with each other in releasing the individual anterior pituitary hormones. When given in combination, the releasing hormones were administered as sequential 20-sec iv infusions in the following order and doses: ovine corticotropin-releasing hormone, 1 microgram/kg; GnRH, 100 micrograms; human GH-releasing hormone, 1 microgram/kg; and TRH, 200 micrograms. Plasma or serum samples were assayed for ACTH, cortisol, GH, PRL, FSH, LH, and TSH at multiple times for 120 min after injection. Compared to individual administration, combined administration of these four hypothalamic releasing hormones caused no apparent inhibition or synergism with respect to the individual hormone responses of these normal subjects. Side-effects of the combined test were the same as those observed with individual hormone administration. No unusual or dangerous side-effects were observed. Having confirmed the efficacy of combined administration of the four releasing hormones, we administered the combination to five additional normal men and 12 normal women. Anterior pituitary hormone and cortisol responses were the same in men and women, except for a lower LH and a greater PRL response in women. There was a rapid increase in all hormones, with peak levels usually reached by 60 min. Adequate assessment of individual hormone responses can be achieved by assaying a basal and only 2 (or 3 in the case of ACTH and GH) postinfusion samples. A rapid, safe, and useful test of combined anterior pituitary function appears to be feasible using these four hypothalamic releasing hormones.
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PMID:Rapid sequential intravenous administration of four hypothalamic releasing hormones as a combined anterior pituitary function test in normal subjects. 298 3

Plasma LH fluctuations reflect pulsatile hypothalamic GnRH activity. In order to investigate a possible interaction between opiate and dopaminergic pathways in the control of LH and PRL release, a met-enkephalin analogue (FK 33-824) was administered intravenously to female volunteers at a rate of 0.01 mg/kg/h for 4 h. LH pulses as recorded by plasma measurements every 20' were significantly (p less than 0.01) inhibited whereas PRL concentrations were increased. Pre-treatment with bromocriptine, 1.25 mg b.i.d. for 3 days, counteracted the stimulatory effect of FK 33-824 on PRL secretion but the inhibitory effect on LH episodic release was not modified by this dopamine agonist. Results indicate that opiate receptor stimulation selectively depresses hypothalamic GnRH activity and enhances PRL release from pituitary lactotrops. The GnRH lowering effect does not seem to be mediated by dopaminergic mechanisms which govern PRL secretion. Also transient, opioid-induced hyperprolactinemia is not causally related to the suppression of hypothalamic GnRH activity.
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PMID:Effect of dopamine receptor stimulation on the inhibition of LH pulsatility by a met-enkephaline (FK 33-824). 298 25

The levels of gamma 3-MSH immunoreactivity (gamma 3MSH-IR), beta-endorphin immunoreactivity (beta-endorphin-IR), ACTH, PRL, and cortisol were determined in 23 patients with cardiac arrest (CA) and in a group of 22 patients consecutively admitted to the Intensive Care Unit (ICU controls). Blood was obtained immediately after CA and at frequent intervals for the next 2 h. In ICU patients, blood was obtained the morning after admission. gamma 3MSH-IR was consistently elevated after CA; it was present in all 23 patients and was detectable in 113 of 114 samples. The mean peak gamma 3MSH-IR level was 162 +/- 20 (+/- SE) pg/ml in CA patients and the mean gamma 3MSH-IR level was 35 +/- 6 pg/ml in ICU controls (P less than 0.01). gamma 3MSH-IR was undetectable (less than 20 pg/ml) in normal subjects. CA also was associated with increases in ACTH, beta-endorphin-IR, cortisol, and PRL. The group of ICU controls had stress hormone levels that were generally within the normal range. Distribution of plasma beta-endorphin-IR by gel chromatography showed two peaks of immunoreactivity corresponding to the beta-endorphin and beta-lipotropin standards in both the CA and ICU control groups. Distribution of gamma 3MSH-IR in CA plasma showed a major peak of immunoreactivity with a mol wt of approximately 6,000 daltons and two minor components of approximately 4,000 and 11,000 dalton. No immunoreactivity coeluted with a gamma 3MSH standard. We conclude that gamma 3MSH-immunoreactive peptides are a consistent component of the massive release of pituitary and adrenal glandular products after CA.
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PMID:gamma 3-Melanocyte-stimulating hormone immunoreactivity is a component of the neuroendocrine response to maximal stress (cardiac arrest). 298 21

Experiments were designed to evaluate the role of activators of protein kinase C, such as 1,2-diacylglycerol and phorbol esters, on the release of all the anterior pituitary (AP) hormones in vitro. Dispersed rat AP cells were incubated in the presence of 1,2-didecanoylglycerol (DiC10), a synthetic diacylglycerol, or phorbol 12,13-dibutyrate (PDBu), a tumor-promoting phorbol ester, at different concentrations and for varying periods of time. ACTH and beta-endorphin (beta-End) secretion were enhanced by DiC10 in a concentration-dependent manner, with a minimal effective concentration of 5 microM. PDBu at 5 nM produced a significant release of both ACTH and beta-End. The effect of DiC10 and PDBu was time dependent, with maximal responses occurring at 15-30 min for DiC10 and 30-60 min for PDBu. Release of GH was also enhanced significantly by DiC10 and PDBu, with minimal effective concentrations of 1 microM and 1 nM, respectively. Maximal release of GH was already attained within 15 min with DiC10 or 60 min with PDBu. In additional experiments, the effects of DiC10 and PDBu on secretion of LH, FSH, PRL, and TSH were evaluated. The results indicate that 5-25 microM DiC10 produced a concentration-dependent release of each of those hormones, and that 5 microM was the minimal effective concentration in every case. Nearly maximal stimulation was achieved within 15 min for each hormone. PDBu (50 nM) significantly enhanced LH, FSH, PRL, and TSH release within 30 min. Although qualitatively all hormones were similarly stimulated, both with respect to time and concentration, some quantitative differences were observed. ACTH and beta-End release were enhanced 100% by DiC10 and 300% by PDBu, whereas the increase in other hormones was of a lesser magnitude. The present study indicates that two specific stimulators of protein kinase C, diacylglycerol and phorbol ester, can enhance secretion of all AP hormones in a concentration- and time-dependent manner. This suggests that formation of endogenous 1,2-diacylglycerol may represent a physiological intracellular messenger in the events leading to AP peptide hormone release.
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PMID:1,2-Didecanoylglycerol and phorbol 12,13-dibutyrate enhance anterior pituitary hormone secretion in vitro. 299 14

Corticotropin releasing factor (CRF) is a newly sequenced peptide first isolated from sheep hypothalami and thought to be an important modulator of both the pituitary-adrenal axis and the sympathetic nervous system. We administered intravenous, intramuscular, and intracerebroventricular CRH to non-human primates and measured plasma ACTH, beta endorphin, cortisol, GH and PRL responses to CRF. In addition, we determined the pharmacokinetic properties of I125 in these primates. We administered CRF as an intravenous bolus or as a continuous infusion to normal volunteers and as an intravenous bolus to patients with disorders of the hypothalamic-pituitary-adrenal axis, such as Cushing's syndrome and adrenal insufficiency, and patients with endogenous depression and mild hypercortisolism, and assessed their plasma ACTH, cortisol, GH and PRL responses. In addition, we determined the pharmacokinetic properties of CRF in man by measuring CRF immunoreactivity in plasma. CRF given intravenously to primates or man is a slowly metabolized, long-acting, secretagogue of ACTH, beta-endorphin and cortisol. When given intracerebroventricularly to primates it stimulates the hypothalamic-pituitary-adrenal axis without escaping into the plasma and it is actively cleared in the CNS. It does not cross the blood brain barrier appreciably when given intravenously. CRF given to primates and men as an intravenous continuous infusion has only mild ACTH stimulating effects and this may be due to an intact cortisol negative feedback system. Finally, CRF causes characteristic plasma hormone responses in patients with Cushing's disease, adrenal insufficiency and depression.
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PMID:Corticotropin releasing factor: basic studies and clinical applications. 299 71

The hormonal and neurochemical responses to acute ether stress, morphine, and/or naloxone were analyzed in infantile (13-day-old) and prepubertal (36-day-old) male CD rats in an attempt to identify a possible neurochemical correlate(s) for the previously demonstrated requisite maturation of the PRL response to ether stress. Neuronal serotonin (5-HT), norepinephrine (NE), and dopamine (DA) activities were examined in the medial preoptic hypothalamic area (MPOH), medial basal hypothalamic area (MBH), and median eminence (ME). Ether stress increased plasma PRL, ACTH, and beta-endorphin-like immunoreactivity (beta end) as well as NE metabolism in the MPOH and MBH and neuronal 5-HT activity in the MBH, and decreased neuronal DA activity in the ME of prepubertal animals. Ether stress elicited similar changes in infantile animals, with the important exceptions that plasma PRL, neuronal 5-HT activity in the MBH, and neuronal DA synthesis in the ME were not affected at this earlier age. Morphine increased plasma PRL, ACTH, and beta end levels, elevated neuronal NE and 5-HT activities in the MPOH and MBH, and decreased DA synthesis in the ME in both infantile and prepubertal animals. Naloxone administration did not alter basal hormone concentrations or neuronal monoamine activity in any brain area, but did prevent all of the morphine-induced changes as well as the ether stress-induced changes in PRL, MBH neuronal 5-HT activity, and DA synthesis in the ME of prepubertal animals. In addition, naloxone augmented the ether stress-induced increases in ACTH and beta end in prepubertal rats. Indirect stimulation of 5-HT neurons by administration of the amino acid precursor of 5-HT, 5-hydroxytryptophan, resulted in decreased DA synthesis in the ME of infantile animals and increased plasma PRL levels in that age group, indicating that this portion of the neurochemical connection is already present in infantile animals. Furthermore, the 5-hydroxytryptophan-induced increase in PRL was blocked by pretreatment with naloxone. The results demonstrate that both the ether stress- and morphine-induced increases in plasma PRL, but not in ACTH or beta end, are associated with increased neuronal 5-HT activity in the MBH and a decreased neuronal DA activity in the ME, that these are opiate receptor-mediated effects, and that infantile rats apparently lack a functional opiate-5-HT connection, which matures some time between days 13 and 36 postnatally.
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PMID:Maturation of the prolactin and proopiomelanocortin-derived peptide responses to ether stress and morphine: neurochemical analysis. 300 67

Controversy surrounds the issue of whether beta-endorphin affects adrenal steroidogenesis. Recent work has both supported and refuted the claim that beta-endorphin stimulates a rise in serum aldosterone. We investigated the role of beta-endorphin in adrenal steroidogenesis by examining its potential modulation of the response of serum cortisol to exogenous ACTH (Cosyntropin). Four of five normal men received: 1) synthetic beta-endorphin (1 microgram/kg X min) for 30 min, followed by a bolus dose of 0.2 micrograms ACTH; 2) beta-endorphin (100 micrograms, iv), followed by 0.2 micrograms ACTH iv; 3) 0.2 micrograms ACTH iv; and 4) beta-endorphin (100 micrograms iv) alone. The integrated cortisol response to exogenous ACTH, calculated as the area under the cortisol response curve, was significantly less when the ACTH infusion was preceded by the 30-min beta-endorphin infusion than when administered alone [163 +/- 50 (SE) microgram/dl X min vs. 282 +/- 51 micrograms/dl X min, respectively; P less than 0.01]. By contrast, there was no difference between the integrated cortisol response to exogenous ACTH alone and exogenous ACTH after the bolus dose of beta-endorphin (282 +/- 51 vs. 293 +/- 39 micrograms/dl X min, respectively). Beta-Endorphin (30-min infusion or 100-micrograms bolus dose alone) caused no change in serum aldosterone, dehydroepiandrosterone, or PRA. Serum PRL levels, however, were raised significantly (P less than 0.05) by the 30-min infusion of beta-endorphin. The infusion and bolus doses of beta-endorphin raised plasma beta-endorphin levels to over 100,000 pg/ml and 5,000 pg/ml, respectively. We conclude that very high plasma levels of beta-endorphin may influence the response of cortisol to ACTH through a direct effect on the adrenal cortex. However, even in disease states such as Addison's and Nelson's diseases, such levels of plasma beta-endorphin are not known to be achieved.
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PMID:Beta-endorphin attenuates the serum cortisol response to exogenous adrenocorticotropin. 300 53

Ten normal young men (22-28 yr of age), within 10% of their ideal body weight, were given the four releasing hormones (TRH, 200 micrograms; GnRH, 100 micrograms; ovine corticotropin-releasing hormone, 50 micrograms; GH-releasing hormone, 80 micrograms) iv on separate days and then in combination on the same day. Plasma TSH, PRL, FSH, LH, cortisol, ACTH, and GH were measured by RIA in samples collected from 20 min before to 120 min after injection. There were no significant differences in responses to the separate and combined tests for FSH, LH, cortisol, ACTH, and GH. The plasma TSH (0.001 less than P less than 0.01) and PRL (P less than 0.001) responses were significantly higher after the combined test. The tolerance was identical to that of TRH alone. In eight patients studied after pituitary surgery, combined administration provided results comparable to those obtained after separate administration of TRH, GnRH, and insulin.
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PMID:Pituitary stimulation by combined administration of four hypothalamic releasing hormones in normal men and patients. 300 59

The ability of two proopiomelanocortin-derived peptides, alpha MSH and corticotropin-like intermediate lobe peptide (CLIP) [ACTH (18-39)] to antagonize the stimulation of PRL secretion by beta-endorphin (beta EP) was studied in the rat. When 50 ng beta EP were injected into the lateral cerebral ventricle, plasma PRL rose from a mean baseline of 1.87 +/- 0.43 ng/ml (+/- SEM) to a peak of 23.0 +/- 3.67 ng/ml 10 min after the injection. When the same animals received 500 ng alpha MSH together with 50 ng beta EP, the peak concentration of PRL was reduced by 74% to 6.05 +/- 1.43 ng/ml (P less than 0.005). After the injection of 500 ng CLIP together with 500 ng beta EP, the peak concentration of PRL was reduced by 47% to 12.8 +/- 3.09 ng/ml (P less than 0.01). Total PRL release, determined by calculating the areas under the plasma PRL concentration curves, was also significantly reduced by the injection of alpha MSH or CLIP. A dose of 100 ng alpha-MSH or CLIP also antagonized the stimulation of PRL secretion by 50 ng beta EP. PRL release was reduced by 62% after administration of 100 ng alpha MSH (P less than 0.001) and by 43% after 100 ng CLIP (P less than 0.05). When 100 ng alpha MSH and 100 ng CLIP were injected together, there was an additive effect in blocking the stimulation of PRL release by beta EP, and the peak plasma PRL concentration was reduced by 81%. Des-acetyl alpha MSH, the predominant form of alpha MSH in the hypothalamus, was also very effective in antagonizing beta EP-induced PRL release. The peak PRL concentration was reduced by 52% after administration of 100 ng des-acetyl alpha MSH plus 50 ng beta EP compared with that after beta EP alone (P less than 0.005). We conclude that relatively low doses of both alpha MSH and CLIP can effectively antagonize the actions of beta EP on pituitary PRL release. These findings suggest the possibility that differential posttranslational processing of proopiomelanocortin may serve as a regulator of anterior pituitary function.
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PMID:Antagonism of beta-endorphin-induced prolactin release by alpha-melanocyte-stimulating hormone and corticotropin-like intermediate lobe peptide. 301 83

Prolactin secretion was investigated in an attempt to identify the patterns of responses in different types of tumors. Forty four patients were studied: thirty patients with prolactinomas (Group 2); nine patients with growth-hormone (GH)-adrenocorticotropic hormone (ACTH)-secreting pituitary tumors and hypothalamic tumors (Group 3); and five patients with non-secreting pituitary tumors (Group 4). A control group (Group 1) consisted of 60 healthy subjects (30 males and 30 females). All were submitted to testing by nomifensine (Nom), domperidone (Dom) and thyrotropin releasing hormone (TRH). The prolactin levels were measured by radioimmunoassay (RIA). In group 2 the suppression of PRL with Nom and the stimulation with Dom and TRH were significantly lower than in the control group (p less than 0.001). There was no statistically significant difference between groups 2 and 3 in the suppression with Nom. The increase with Dom in group 3 was significantly greater than that in group 2 (p less than 0.001) and less than that in the control group (p less than 0.005). The rise in PRL with TRH was also significantly higher in group 3 than in group 2 (p less than 0.001) and similar to that of the control group. Group 4 gave the same results as the control group to all 3 tests. Our results indicate a dopaminergic irregularity in the hypothalamic and GH-ACTH-secreting pituitary tumors, thus supporting a hypothalamic etiopathogenesis of these tumors. The normality of the GH-ACTH-secreting pituitary tumors and hypothalamic tumor responses to TRH is one more factor in differentiating these from prolactinomas. The normal response of the non-secreting tumors may involve a primary pituitary etiology of these tumors.
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PMID:Evidence of abnormal dopaminergic control of prolactin in patients with hypothalamic and pituitary tumors. 303 40


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