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 number of sites have been hypothesized as loci at which opioid substances act to alter the secretion of luteinizing hormone (LH) and prolactin (PRL) (1-8). The aim of the present study was to determine the site(s) at which the opioid peptide beta-endorphin (beta-END) acts to influence plasma LH and PRL levels in the ovariectomized (OVX) rat. beta-END, administered into the third ventricle of conscious OVX rats fitted with jugular catheters, significantly decreased plasma LH in doses greater than or equal to 50 ng and increased PRL levels at all doses administered (10, 50, 100 and 250 ng) in a dose dependent fashion. To identify possible central nervous system sites of action, 250 ng beta-END was unilaterally infused into various brain sites. Plasma LH was significantly decreased and plasma PRL significantly increased by infusions into the ventromedial hypothalamic area, the anterior hypothalamic area, and the preoptic-septal area. There was no significant effect of beta-END infusions into the lateral hypothalamic area, amygdala, midbrain central gray, or caudate nucleus. When hemipituitaries of OVX rats were incubated in vitro with beta-END (10(-7)M to 10(-5)M), there was no suppression of basal or LHRH-induced LH release, nor was there any alteration of basal PRL release. It is concluded that beta-END acts at a medial hypothalamic and/or preoptic-septal site and not the pituitary, to alter secretion of LH and PRL.
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PMID:Site of action for beta-endorphin-induced changes in plasma luteinizing hormone and prolactin in the ovariectomized rat. 632 5

We have investigated the in vitro and in vivo interactions of the four hypothalamic releasing factors, LHRH, corticotropin-releasing factor, TRH, and GH-releasing factor on anterior pituitary hormone secretions, using a 2 X 2 X 2 X 2 factorial experimental design. This experimental design allows for the evaluation of both the main treatment effects of the hypothalamic releasing factors as well as all of the possible interactions between them. Significant main treatment effects were: LHRH on LH and FSH, corticotropin-releasing factor on ACTH and beta-endorphin, TRH on TSH, and GH-releasing factor on GH. These results confirm the specificity of the four releasing factors on their respective target cells. There were no significant interactions between any of the releasing factors on anterior pituitary hormone secretions. These results suggest that the changes in pituitary secretion that are observed under physiological conditions are not due to interactions between the hypothalamic releasing factors at the level of the pituitary, but rather to other secondary interactions that modify pituitary activation or response. These results also indicate that the clinical pituitary reserve tests can be expanded to include all four hypothalamic releasing factors, since any lack of response will reflect a specific pituitary defect and not a failure to respond owing to interaction of the secretagogues administered.
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PMID:Multiple stimulation of the adenohypophysis by combinations of hypothalamic releasing factors. 632 31

The purpose of this study was to evaluate the effect of chronic immobilization on the hypophysial-adrenal and hypophysial-gonadal axes of adult male rhesus monkeys and the effect such manipulation has on the ability of these axes to respond to exogenous corticotropin, gonadotropin, and GnRH administration. A comparison was also made of the effects of immobilization on testosterone secretion at periods of low (April) and high (November) gonadal activity in this animal. Adult male rhesus monkeys were immobilized in a horizontal position for periods of up to 20 days during March/April. The function of the hypophysial-adrenal and hypophysial-gonadal axes was studied by monitoring plasma levels of cortisol, 17-hydroxylated precursors, 11 deoxycortisol, and testosterone during the period of restraint. Groups of immobilized and control animals also received iv injections of ACTH, FSH, and LH or LHRH on day 18 of the experiment. An additional group of animals was immobilized for 20 days, but did not receive exogenous hormone treatment. This group was used for comparison of seasonal differences in testosterone secretion with another group of animals subjected to the same treatment in November. During the first 3 h of immobilization, levels of cortisol, 17-hydroxylated precursors, and 11-deoxycortisol increased markedly from initial levels. Cortisol levels remained elevated for 3 days, whereas levels of the other three adrenal hormones declined to near-initial levels within 24 h. Testosterone levels declined steadily during the first 6 h of immobilization in males studied at a time of high testicular activity (November), while an increase during the first hour of restraint followed by a decline during the next 3 days were observed in males studied during a period of low testicular activity (April). Animals injected with ACTH on day 18 of immobilization had cortisol levels similar to those of control animals, but other groups of animals restrained for a similar period exhibited a lower level of plasma testosterone than controls after the injection of FSH and LH or LHRH. These data suggest that adaptation to stress results in a reduced demand for corticosteroid production and that the adrenals of chronically stressed animals are capable of responding to exogenous corticotropin, or alternatively, the immobilization imposed was stressful for only a limited time, and after a few days, animals no longer reacted as in response to stress. Also, secretion of testosterone in male monkeys is markedly influenced by the functional state of the gonads at the time of stress initiation.
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PMID:Levels of adrenal and gonadal hormones in rhesus monkeys during chronic hypokinesia. 632 44

The glandular origin of excess circulating steroid hormones in women with polycystic ovarian disease has been difficult to establish with previously described perturbation techniques. Recently it was demonstrated that daily administration of a potent gonadotropin-releasing hormone agonist achieves complete and reversible suppression of ovarian steroid secretion. To examine the source of C-21 steroid hormones, circulating levels were measured before and after administration of the same agonist in polycystic ovarian disease subjects and normal control subjects. Serum levels of these hormones were also determined after administration of dexamethasone and adrenocorticotropic hormone (ACTH) as well as bilateral oophorectomy. Subjects with polycystic ovarian disease exhibited significant elevations of serum pregnenolone, 17OH -pregnenolone, and 17OH -progesterone by comparison with normal control subjects. The glandular origins of the excess levels of pregnenolone and 17OH -pregnenolone were more difficult to determine and appear to be different from that of 17OH -progesterone.
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PMID:Origin of serum progestins in polycystic ovarian disease. 633 Jun 31

The axonal projections of cell groups containing the most dense collections of steroid hormone concentrating cells have been demonstrated with retrograde neuroanatomical tracing methods. Horseradish peroxidase revealed large numbers of neurons in ventrolateral ventromedial nucleus (VL-VM) which project to dorsal midbrain. Wheat germ agglutinin (immunocytochemical recognition method) revealed large numbers of neurons in medial basal hypothalamus (MBH) and particular subdivisions of paraventricular nucleus (PVN) that project to dorsal caudal medulla or spinal cord. Fluorescent dyes revealed that many preoptic area (POA), anterior hypothalamic (AHA), and bed nucleus of the stria terminalis (BNST) neurons project to ventral tegmental area of Tsai (VTA). Also many neurons in POA and BNST project to amygdala. A method which enabled simultaneous demonstration of the steroid binding capacity and axonal projections of neurons in the same tissue section revealed that 26-36% estradiol (E2) concentrating cells in VL-VM project to dorsal midbrain. E2 concentrating neurons in POA and BNST project to amygdala and E2 concentrating POA neurons project to VTA. These neurons, which send their axons to cell groups located in different brain regions, are probably under the genomic-regulatory influence of E2. Using a method which allows simultaneous demonstration of peptide content and steroid hormone concentrating capacity of cells, many oxytocin-neurophysin and vasopressin-neurophysin containing magnocellular neurons in the caudal PVN were found to concentrate E2. About 4% of the beta-endorphin and about 6% of the dynorphin containing neurons in the MBH concentrate E2. In contrast, virtually none (less than 0.2%) of the LHRH containing hypothalamic neurons concentrate E2.
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PMID:Axonal projections and peptide content of steroid hormone concentrating neurons. 638 52

We have developed and used a sensitive and specific radioimmunoassay to demonstrate the presence of CRF-like immunoreactivity in extra-hypothalamic areas of ovine brain. Synthetic CRF displaced antibody bound tracer at an ED50 value of 200 pg and there was no cross-reactivity with LHRH, TRH, ACTH, beta-endorphin and several other peptides. Displacement of bound 125I-CRF by brain extracts exhibited curves parallel to synthetic CRF standards. Highest concentrations (1 ng/mg tissue) of CRF-like immunoreactivity were found in the median eminence but surprisingly, high concentrations of CRF-like immunoreactivity were found in frontal, parietal, occipital and particularly temporal areas of cerebral cortex. Much lower concentrations were found in other brain areas including the basal ganglia, limbic system and brain stem.
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PMID:Distribution of corticotropin-releasing factor in ovine brain determined by radioimmunoassay. 660 Aug 47

This paper reports an immunofluorescent study of the pituitary in the fetal pig (Sus scrofa). Fifteen antisera were used against most of the hormones present in the pituitary. Five types of hypophysial endocrine cells were observed in the anterior and intermediate lobes. We determined the sequential appearance of these various cell types in the fetus. The first hormones found at 33 days were ACTH, beta-MSH, beta- and gamma-LPH and alpha- and beta-endorphin; alpha-MSH appeared at 40 days and STH at 45 days. The glycoprotein hormones, LH (45 days), TSH (50 days) and FSH (60 days), appeared between 45 and 60 days. The density and staining of the gonadotropes increased up to 80 days, at which time they reached values similar to those of the adult. Prolactin was not found until 80 days. An anti-LHRH antiserum was used to study LHRH neuron differentiation between 30 and 70 days of pregnancy. The first immunoreactive perikaryons were found at 40 days but the immunoreactive fibers did not reach the median eminence until about 60 days. However, we observed differentiated capillary loops in the palisade layer of the median eminence only in the 70-day fetus. These results when compared with actual data on the differentiation of the reproductive function in the pig fetus permitted us to define an overall pattern of the differentiation and functioning of the fetal neuroendocrine hypothalamo-pituitary-gonadal system in the porcine species. This pattern includes, (i) autodifferentiation and autofunctioning of the gonads and (ii) autodifferentiation of the pituitary with (iii) later assumption by the hypothalamus followed by a phase during which the whole reproductive system functions.
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PMID:Immunocytological study of the chronology of pituitary cytogenesis in the domestic pig (Sus scrofa) with special reference to the functioning of the hypothalamo-pituitary-gonadal axis. 676 Feb 97

The effect of long-acting analogue of met-enkephalin (DAMME) and naloxone on gonadotrophin secretion has been investigated in man. In menopausal women DAMME induced a progressive fall in LH to approximately 60% of basal levels at 3 h, which was blocked by naloxone; there was a smaller fall in FSH that did not attain statistical significance. However, the LHRH-induced rise in LH and FSH in young male volunteers was unaffected by pretreatment with a high-dose DAMME infusion. Naloxone infusion in young male and female normal subjects produced a significant rise in both LH and FSH. Long-term infusion of naloxone appeared to increase the rate, and possibly the amplitude, of LH pulsatility. These results suggest that met-enkephalin-like opioid peptides exert a tonic inhibitory control of LH release in both menopausal and young subjects of both sexes. This control is most likely to be at the level of the hypothalamus, and involves modulation of pulsatile LHRH release.
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PMID:The opioid control of LH and FSH release: effects of a met-enkephalin analogue and naloxone. 678 82

Sixteen peptides were injected intracerebroventricularly to test their effects on rectal temperature of rabbits in a thermoneutral environment. In initial tests 5 micrograms alpha-MSH, ACTH(1--24), oxytocin, vasopressin and glucagon altered body temperature while ACTH(1--10), cholecystokinin, contraceptive tetrapeptide, gastrin, insulin, interferon, leupeptin, LHRH, panhibin (somatostatin), and proctolin did not. Bombesin also altered body temperature but in no consistent direction. In further tests on the effective peptides 1.25--5.0 micrograms alpha-MSH and ACTH(1--24) produced dose-related decreases in rectal temperature as great as 1.0 degrees C. The same doses of oxytocin and glucagon produced small, prolonged hyperthermias which did not exceed 0.4 degrees C. Vasopressin caused rapid development of small increases in rectal temperature; temperature returned to normal in 2--3 hr. The results suggest that five of the peptides tested may have roles in central mediation of normal body temperature, hypothermia, hyperthermia and fever.
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PMID:Central administration of peptides alters thermoregulation in the rabbit. 724 7

The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m2) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 micrograms) + thyrotropin-releasing hormone (TRH, 200 micrograms) + luteinizing hormone-releasing hormone (LHRH, 100 micrograms) + corticotropin-releasing hormone (CRH, 100 micrograms), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 micrograms) in saline (100 ml) or saline (100 ml) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 micrograms/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 micrograms/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 micrograms/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 micrograms/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 micrograms/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LH, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiological role of galanin in the regulation of anterior pituitary function in humans. 750 94


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