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)

Specific somatostatin (SRIH) receptors on human pituitary adenoma cell membranes were characterized using [125I]Tyr11-SRIH as the radioligand. Specific binding of [125I] Tyr11-SRIH to adenoma cell membranes reached a steady state within 30 min at 25 C, and semilogarithmic analysis of the data revealed that the rate of the binding was linear at 25 C with a t1/2 of 13.2 min. Specific binding increased linearly with 5-160 micrograms plasma membrane protein. SRIH-14 and SRIH-28 inhibited [125I]Tyr11-SRIH binding to adenoma cell membranes with ID50S of 0.32 and 0.50 nM, respectively, while secretin, glucagon, gastrin, cholecystokinin-8, bombesin, TRH, LHRH, human GH-releasing factor-(1-44)-NH2, D-Ala2-met-enkephalin, gamma-aminobutyric acid and taurine did not significantly inhibit binding. All of 13 GH-secreting adenomas investigated had specific and high affinity SRIH receptors, with a dissociation constant (Kd) of 0.80 +/- 0.15 nM (mean +/- SEM) and a maximal binding capacity (Bmax) of 234.2 +/- 86.9 fmol/mg protein (mean +/- SEM). Among five of the nonsecreting pituitary adenomas examined, two had SRIH receptors with Kd values of 0.18 and 0.32 nM and Bmax values of 17.2 and 48.0 fmol/mg protein, respectively. In the remaining three, SRIH receptors were not detected. These results indicate that GH-secreting adenomas as well as some nonfunctioning adenomas have specific SRIH receptors, and hence, the function of the adenomas could be altered by SRIH.
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PMID:Specific somatostatin receptors on human pituitary adenoma cell membranes. 286 81

LHRH has previously been found to be the only known hypothalamic releasing factor which can specifically stimulate the release of the opioid dynorphin and other proenkephalin B-derived peptides from the rat adenohypophysis in vitro. In the present study the mechanisms that regulate dynorphin release were further characterized. It was examined whether or not dynorphin release from the adenohypophysis in vitro is altered during inhibition of the secretion of various anterior pituitary hormones. Rat anterior pituitary quarters were incubated in vitro and hormone release into the incubation medium was measured by RIAs. Somatostatin, dopamine, T3, dexamethasone, and 5 alpha-dihydrotestosterone were used to inhibit the secretion of GH, PRL, TSH, ACTH/beta-endorphin, or LH/FSH, respectively. GH, PRL, or beta-endorphin release was inhibited without affecting the simultaneous release of dynorphin A-(1-13)-like immunoreactivity (Dyn A1-13-IR). Concentrations of T3, somatostatin, or dopamine which were effective in suppressing the evoked and/or basal release of TSH, GH, or PRL, respectively, produced no effect on Dyn A1-13-IR release caused by high potassium concentration (40 mM) or LHRH (500 pM). The LHRH-induced release of LH and FSH was inhibited by the glucocorticoid dexamethasone or the androgen 5 alpha-dihydrotestosterone. Under these conditions, Dyn A1-13-IR release was also reduced. However, whereas LH release was completely blocked by 5 alpha-dihydrotestosterone, FSH and Dyn A1-13-IR release was reduced only by 50%. The release of FSH and Dyn A1-13-IR in vitro from anterior pituitary glands taken from rats, castrated 3 weeks before, was enhanced to a similar extent (about 2.5-fold); the simultaneous enhancement of LH release was significantly (P less than 0.005) greater (about 5-fold). We conclude that the mechanisms which regulate the release and/or biosynthesis of dynorphin and other proenkephalin B-derived peptides of the adenohypophysis are similar to those of the gonadotropins but different from those of any other anterior pituitary hormone, and may be more closely related with FSH release than LH release. These data support the view that dynorphin of the normal rat adenohypophysis may be localized in at least a subpopulation of gonadotrophs.
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PMID:Release of dynorphin-like immunoreactivity from rat adenohypophysis in vitro during inhibition of anterior pituitary hormone secretion from individual cell types. 288 74

During the last few years, many neuropeptides have been isolated, characterized and synthesized. Neuroendocrinology is one area in which there has been major progress, particularly through the isolation of two new hypothalamic factors, corticotropin releasing factor (CRF) and growth hormone releasing factor (GRF). CRF specifically stimulates pituitary secretion of ACTH and other peptides derived from pro-opiomelanocortin (beta-lipotropin, beta-endorphin), while GRF, together with somatostatin, controls secretion of the growth hormone. Knowledge of the structures of the hypothalamic factors has allowed the synthesis of the native substances as well as many potent analogues with agonist and antagonist properties. These substances have numerous clinical applications. LHRH or its analogues are presently used or being tested in various conditions such as treatment of hormone-related cancers (prostate, breast), endometriosis, idiopathic precocious puberty as well as in sterility problems. The recent availability of long acting somatostatin analogues has raised great therapeutic expectations in various endocrine and digestive diseases. Whereas GRF can be used in the treatment of short stature, CRF has so far not been shown to be a potential important therapeutic agent. However, its clinical application as a diagnostic test is clearly useful in many situations. There is a promising future for the clinical applications of these substances in various endocrine, digestive and perhaps in psychiatric diseases, and in hormone-related cancers.
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PMID:[Hypothalamic factors: recent diagnostic and therapeutic advances]. 289 Feb 1

The effect of dynorphin A-(1-13) (Dyn A-(1-13] and other opioids on the cytosolic free calcium concentration [(Ca2+]i) in rat anterior pituitary cells was examined using the fluorescent indicator fura-2. A commercial synthetic Dyn A-(1-13) preparation elevated [Ca2+]i. Results, which were obtained with receptor antagonists, and in LHRH receptor radioligand binding studies as well as by HPLC combined with LHRH radioimmunoassay, strongly suggest that this effect of the dynorphin preparation was due to contamination with a LHRH-like compound. Dyn A-(1-13), purified by HPLC, as well as Dyn A-(2-13), [Leu5]enkephalin, beta-endorphin, morphine, or U50,488H had no effect on [Ca2+]i. LHRH caused a rapid increase in [Ca2+]i by about 50 nM which was blocked by the LHRH antagonist, [D-pGlu1,D-Phe2,D-Trp3,6] LHRH.
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PMID:Opioids and cytosolic calcium in rat anterior pituitary: dynorphin preparation showed LHRH-like action due to contamination. 290 77

Four tumors consisting of pituitary adenomatous cells (AD) intricated with ganglion cells (GC) were studied. Each case was associated with a different clinical syndrome: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome with no hormonal hypersecretion. (a) In the case with acromegaly, immunoreactive growth hormone (IR-GH) was present in 80% of AD. IR-vasoactive intestinal peptide (VIP) was found in 5%-10% of AD and in few GC. Rare GC and processes showed IR-GH-releasing hormone (GRH), -somatostatin (SRIH), -gonadotropin-releasing hormone and -adrenocorticotropin-releasing hormone. (b) In the case with amenorrhea-galactorrhea, IR-prolactin (PRL) was seen in 90% of AD. IR-PRL and -VIP were present in rare GC. (c) In the case with Cushing's disease, 60% of AD and very few GC contained IR-adrenocorticotropin (ACTH) and beta-lipotropin. Rare GC processes contained IR-SRIH. (d) In the case without pituitary hormone hypersecretion, PRL was localized in rare AD and GC. Pituitary hormone and neuropeptides were never colocalized in the same cells. No case displayed IR-neurophysins or -thyroliberin. Pituitary hormones were localized by ultrastructural immunogold labeling. These findings show that: (i) in three cases, pituitary hormones (PRL and ACTH), and, in one case, VIP could be localized in both adenomatous and ganglion cells; (ii) the pituitary hormone-containing cells in the tumors could be related to the hypersecretory syndromes; (iii) intratumoral IR-VIP and -GRH might be involved in GH and PRL hypersecretion in the cases with acromegaly and amenorrhea-galactorrhea.
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PMID:Immunocytochemistry of four mixed pituitary adenomas and intrasellar gangliocytomas associated with different clinical syndromes: acromegaly, amenorrhea-galactorrhea, Cushing's disease and isolated tumoral syndrome. 292 94

To study the effect of human beta-endorphin (beta h-End) on pituitary response to gonadotropin-releasing hormone (LH-RH) and thyrotropin-releasing hormone (TRH) in vitro, we used dispersed rat pituitary cells. When beta h-End (10(-7) M) was simultaneously added along with LH-RH, its stimulatory effect was blocked and naloxone (NAL, 10(-5) M) did not reverse the beta h-End inhibitory effect. NAL alone elicited an increase in LH release, but in the presence of both stimulants (LH-RH and NAL), LH secretion was lower than that observed with LH-RH alone. TRH stimulatory activity of TSH and PRL secretion was blunted by the presence of beta h-End (10(-7) M) and was not reversed by NAL (10(-5) and 10(-3) M). These data suggest that beta h-End directly blocks the LH, TSH- and PRL-secreting activity of both LH-RH and TRH at the pituitary level. This beta h-End effect is not reversed by the specific opiate receptor blocker NAL.
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PMID:Inhibitory effect of beta-endorphin on gonadotropin-releasing hormone and thyrotropin-releasing hormone releasing activity in cultured rat anterior pituitary cells. 294 10

In vivo single-unit extracellular recording was used to assess neuronal membrane sensitivity at the level of the midbrain central gray (MCG) to the iontophoresis of luteinizing hormone releasing hormone (LHRH) and beta-endorphin (beta-END). The percentage of change in firing rate was evaluated to determine the effect of exogenously administered estradiol benzoate (EB) and EB plus progesterone (EB + P) on the membrane sensitivity of these MCG neurons to LHRH and beta-END. Ovariectomized adult female rats were primed with EB or EB + P, or nonprimed, 24-48 h prior to recording. EB priming significantly altered the membrane sensitivity of neurons in the MCG to LHRH by increasing the number of cells excited compared to the EB + P group and the nonprimed controls (p less than 0.005). The addition of P appeared to negate this effect. Hormonal priming did not alter the response profile for beta-END iontophoresis. The results suggest an estrogen-dependent sensitivity to LHRH at the MCG which translates into an increased electrical output, ultimately facilitating lordosis behavior. P treatment dampens this excitation. beta-END's effect on neuronal membrane excitability at the MCG was not distinctly characterized under the hormonal conditions our study evaluated and may reflect a regulatory role under physiological extremes.
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PMID:Estrogen priming affects the sensitivity of midbrain central gray neurons to microiontophoretically applied LHRH but not beta-endorphin. 295 30

An in-vitro superfusion system was used to study the effects of the endogenous opioid peptides [Met]-enkephalin (and its long-lasting analogue [D-Ala2,Met]-enkephalinamide), [Leu]-enkephalin and beta-endorphin and of the opiate antagonist naloxone, on the secretion of LHRH from the mediobasal hypothalamus of the cockerel. The effects of the compounds on both basal release of LHRH and on release stimulated by a depolarizing pulse of increased extracellular potassium ion (64 mmol/l) were investigated. None of the endogenous opioid peptides altered basal release of LHRH; however, both [Met]-enkephalin (10 mumol/l) and [D-Ala2,Met]-enkephalinamide (1 mumol/l) significantly (P less than 0.05) reduced the response to depolarization. Neither [Leu]-enkephalin nor beta-endorphin (0.1-10 mumol/l) were effective. Naloxone (1 mumol/l) administered alone significantly (P less than 0.05) increased basal release of LHRH and abolished the inhibitory effects of [Met]-enkephalin and [D-Ala2,Met]-enkephalinamide on depolarization-induced release. These results suggest that the endogenous opioid peptides exert a tonic inhibitory influence on LHRH secretion by the mediobasal hypothalamus of the cockerel.
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PMID:Modulation by endogenous opioid peptides of the secretion of LHRH from cockerel (Gallus domesticus) mediobasal hypothalamic tissue. 295 76

Immunoreactive and bioactive luteinizing hormone (LH) has been shown to be widely distributed in the rodent central nervous system (CNS), particularly in the hypothalamus. Subcellular localization of this LH in fractions rich in synaptosomes and in vitro release by potassium-induced depolarization suggests that this peptide may act in trans-synaptic neuromodulatory roles. Furthermore, a variety of experiments have proved that this brain-based LH is not of pituitary origin. In the in vitro studies reported here characterization of brain-based LH release, in response to gonadotropin-releasing hormone (GnRH), beta-endorphin, and biogenic amines, was examined. Adult male rats were sacrificed by decapitation, hypothalami removed, quartered, and incubated in Krebs Ringer's Bicarbonate (KRB). High potassium concentration and GnRH induced release of LH from these hypothalamic explants in short-term culture and serotonin significantly inhibited release of LH from these explants. In contrast, however, beta-endorphin, norepinephrine, dopamine, and acetylcholine, agents known to modulate pituitary LH release, had no effect on the release of LH from hypothalamic tissues in vitro. Furthermore, beta-endorphin did not alter potassium-induced release of LH from the hypothalamus. Whereas there are some similarities between LH release from the pituitary and from the CNS, the differences reported here suggest that hypothalamic LH does not simply serve as a supplemental source for LH in the general circulation but more likely subserves an entirely different role(s) than its pituitary counterpart, presumably acting in a neuromodulatory fashion within the brain.
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PMID:In vitro LH release from the hypothalamus-pars tuberalis; effects of gonadotropin-releasing hormone (GnRH), beta-endorphin and biogenic amines. 296 55

A melatonin-induced supersensitivity of the gonadotropin-secretory system to the negative feedback action of sex steroids is thought to be important to the timing of seasonal reproduction. However, little is known concerning this action of melatonin. In the present study the antigonadal action of melatonin in the anterior hypothalamus (AH) of the white-footed mouse, Peromyscus leucopus, was used to examine the neuroendocrine mechanism whereby melatonin enhances the sensitivity to sex steroid negative feedback. Mice received a melatonin-containing pellet in the AH for 14 weeks, at which time they were castrated and treated sc with a Silastic testosterone (T) capsule for 3 weeks. At the time of castration, weight of the testes and the concentration of T in the blood of mice with a melatonin pellet were greatly reduced compared to mice with a blank (melatonin-free) implant in the AH (P less than 0.01). In mice treated with melatonin the physiological dose of T significantly reduced the concentrations of LH in blood and pituitary (P less than 0.05). This dose of T, however, had little effect on LH in mice with a blank pellet in the AH. Melatonin in the AH markedly increased the content of gonadotropin-releasing hormone (GnRH) in the mediobasal hypothalamus (P less than 0.05) in mice treated with T; however, there was little effect of melatonin and/or T in any other region examined. Melatonin and T had little effect on the contents of immunoreactive beta-endorphin (B-EP) in the hypothalamus, but T alone increased the content of B-EP in the preoptic area. These results are evidence that melatonin and T act in concert to induce the reproductively-quiescent state by suppressing secretion of GnRH from the hypothalamus.
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PMID:Melatonin acts in the brain to mediate seasonal steroid inhibition of luteinizing hormone secretion in the white-footed mouse (Peromyscus leucopus). 296 12


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