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)

The beta-endorphin hypothesis of late luteal phase dysphoric disorder (premenstrual syndrome or L2D2) was tested. Twenty-two PMS patients were compared to twenty-two controls. Levels of beta-endorphin, ACTH, FSH, LH, cortisol, prolactin and TRH were measured on the first and twentieth days after menses. PMS subjects exhibited a significantly greater drop in the opiate, beta-endorphin, (p less than .001) than controls. No relationship or significant e was seen with the other hormones/transmitters tested. The symptoms of PMS may be due to noradrenergic rebound following beta-endorphin decline. Symptomatic and pharmacological morphine withdrawal and manic phase of bipolar disorder are discussed as possible models for L2D2.
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PMID:Beta-endorphin decline in late luteal phase dysphoric disorder. 226 89

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

The pathophysiological consequences of endorphin release in anaphylactic shock were investigated through pharmacological studies using opiate antagonists (naloxone, naltrexone, natrexone methyl bromide) as well as agonists (morphine, beta-endorphin). These studies suggest that induction of anaphylaxis provokes the release of endogenous opioids, possibly from the hypothalamus, which contribute to the shock process by stimulating opiate receptors in the CNS. The mechanism of pathophysiologic action of endorphin in anaphylaxis involves, at least in part, inhibition of the central component of the sympatho-adrenalmedullary system. This results in reduced effectiveness of the sympathetic system to physiologically reverse the circulatory effects of the toxic mediators of anaphylaxis. Naloxone, by blocking endorphin action at CNS opiate receptors located at autonomic regulatory centers (e.g. hypothalamus), reverses the sympatho-inhibitory effect of the endorphin peptides. This results in increased central sympathetic outflow to peripheral sympathetic neuroeffector mechanisms; it affords improved sympathetic compensatory responses and increases survival. TRH and DT gamma E physiologically oppose the action of endorphins upon the autonomic system. They stimulate central sympathetic mechanisms through their own receptor systems and increase outflow to peripheral sympathetic effectors. This also results in improved circulatory function and survival.
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PMID:Anaphylactic shock: catecholamine actions in the responses to opioid antagonists. 245 93

Modulation of the activity of K+ channels by TRH and the possible involvement of this modulation in TRH-induced release of alpha-MSH were studied in cultured frog melanotrophs, using patch-clamp and perifusion techniques. Pars intermedia cells were enzymatically dispersed and cultured in Leibovitz medium. In order to test the viability of cultured cells, the amount of alpha-MSH released into the medium was measured by radioimmunoassay every day for 1 week of culture. The total amount of alpha-MSH released during the first 4 days of culture was 8.6 times higher than the intracellular content of alpha-MSH on day 1. Melanotrophs were identified by an indirect immunofluorescence technique using a specific antiserum to alpha-MSH. Recordings obtained in whole-cell, cell-attached and excised patch-clamp configurations showed that TRH induced a transient polarization concomitant with an increase in the probability of opening of Ca2+-activated K+ channels. This transient response was followed by a depolarization accompanied by an enhanced frequency of action potential discharge. TRH also induced a decrease in voltage-dependent K+ conductance. Application of tetraethylammonium, a K+ channel blocker, depolarized the cells and increased the basal secretory level without noticeable changes in TRH-evoked alpha-MSH release. These results demonstrate that the neuropeptide TRH both stimulates Ca2+-sensitive K+ channels and inhibits voltage-dependent K+ current in pituitary melanotrophs. Our data indicate that TRH-induced secretion of alpha-MSH is not a direct consequence of the lowering of K+ conductance. It thus appears that basal and TRH-induced alpha-MSH release occur through distinct pathways; the spontaneous release of alpha-MSH is probably linked to membrane potential, while modulation of the electrical activity is not directly involved in TRH-induced activation of the secretory process.
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PMID:Dual effects of thyrotrophin-releasing hormone (TRH) on K+ conductance in frog pituitary melanotrophs. TRH-induced alpha-melanocyte-stimulating hormone release is not mediated through voltage-sensitive K+ channels. 251 51

In this study, we demonstrated that the cell content and basal secretion of vasoactive intestinal peptide (VIP) in primary rat pituitary cell cultures were increased in hypothyroidism. VIP release from hypothyroid pituitary cells in vitro was stimulated by thyrotropin releasing hormone (TRH 10(-8) to 10(-6) M) and growth hormone (GH)-releasing hormone (GHRH 10(-9) to 10(-8) M) but not by corticotropin-releasing hormone or luteinizing hormone-releasing hormone in concentrations up to 10(-6) M. In the presence of anti-VIP antisera, there was a significant decrease in basal prolactin secretion from cultured hypothyroid pituitary cells (p less than 0.005) indicating that VIP exerts a tonic stimulatory effect on prolactin (PRL) secretion. The increment in PRL secretion following TRH was not affected by exposure to anti-VIP indicating that PRL release after TRH is not mediated by VIP at the pituitary level. In contrast to changes in PRL, exposure to anti-VIP had no effect on basal GH secretion, indicating that the PRL changes are hormone specific. Similarly, GHRH-induced GH release was unaffected by VIP immunoneutralization.
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PMID:Pituitary vasoactive intestinal peptide regulates prolactin secretion in the hypothyroid rat. 251 93

The release of immunoreactive (ir) alpha-MSH and ir ACTH from goldfish (Carassius auratus) melanotropes was investigated using superfused isolated dispersed neurointermediate lobe cell columns. Stimulation of neurointermediate lobe cell columns with pulses of TRH evoked dose-dependent increases in the concomitant release of ir alpha-MSH and ir ACTH. Reversed-phase high performance liquid chromatography (RP-HPLC) was used to characterize the alpha-MSH and ACTH immunoreactivities released from a neurointermediate cell column under spontaneous release conditions. Six peaks of ir alpha-MSH were revealed. Three of these peaks were identified as des-acetyl alpha-MSH, mono-acetyl alpha-MSH and di-acetyl alpha-MSH. Seven peaks of ir ACTH were revealed. Four of these peaks were tentatively identified as ACTH variants. These studies suggest that TRH stimulates the release of peptide hormones from teleost melanotropes and that the goldfish neurointermediate lobe in vitro releases numerous peptides derived from POMC.
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PMID:TRH stimulates the release of POMC-derived peptides from goldfish melanotropes. 255 98

The combined intravenous injection of TRH and GnRH elicited paradoxical responses of plasma beta-endorphin in active and successfully treated pituitary dependent Cushing's disease as well as in ectopic ACTH syndrome and in congenital adrenal hyperplasia. No response was observed in Cushing's syndrome due to adrenal tumours. It is concluded that an abnormal response to inappropriate releasing hormones cannot verify the existence of a pituitary corticotrophic microadenoma.
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PMID:Paradoxical response of plasma beta-endorphin to combined administration of TRH and GnRH in adrenal disorders. 255 25

Seven cases with uremia (6 men, 1 woman, mean age = 55.6 +/- 2.2 years) were studied with four combined hypothalamic releasing hormones (corticotropin-releasing hormone, CRH; luteinizing hormone-releasing hormone, LHRH; thyrotropin-releasing hormone, TRH; and growth hormone-releasing hormone, GHRH) for assessment of anterior pituitary functions. The mean basal levels of corticotropin (ACTH, 22.4 +/- 5.2 pg/ml), thyrotropin (TSH, 2.4 +/- 0.6 microU/ml), and follicle stimulating hormone (FSH, 26.0 +/- 3.4 mIU/ml) in uremic patients were not significantly different from those (34.0 +/- 3.5 pg/ml, 2.0 +/- 0.4 microU/ml, and 23.2 +/- 6.4 mIU/ml) of controls (5 men, 1 woman, mean age = 54 +/- 2.5 years), but the ACTH and TSH responses to the releasing hormones were significantly lower than those of the controls. The mean basal levels of luteinizing hormone (LH, 70.7 +/- 16.3 mIU/ml), cortisol (9.8 +/- 1.2 micrograms/dl) and prolactin (109.3 +/- 23.2 ng/ml) in uremic patients were significantly higher than those of normals (27.3 +/- 6.6 mIU/ml, 6.5 +/- 0.7 micrograms/dl and 15.7 +/- 3.4 ng/ml), while suppressed LH, cortisol and prolactin responses to the releasing hormones were observed in the uremic group. The mean basal growth hormone (GH) level in uremic patients (3.1 +/- 0.4 ng/ml) was not significantly different from that (2.8 +/- 0.7 ng/ml) of normals, but the GH response to the releasing hormones was significantly higher than that of controls. These results show pituitary dysfunction, such as blunted ACTH, TSH, LH and prolactin response, exists in uremic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anterior pituitary functions in patients with uremia tested by stimulation with four combined hypothalamic releasing hormones. 256 85

Culturing sympathetic ganglion neurons in vitro may modify phenotypic expression of some neurotransmitters. For dorsal root ganglia (DRG), contradictory results have been reported; most studies have used immature material. We have therefore performed a detailed immunocytochemical analysis of the transmitter content of cultured adult rat DRG neurons. To demonstrate possible modifications of neurotransmitter phenotypes, we have compared the results obtained with the same techniques on neurons cultured for 3 days and on freshly dissociated DRG cells. Also, the transmitter profile of cultured neurons was compared with that known from in situ studies. Out of 22 antigens studied, 20 were detected in cultured DRG neurons. All of them were expressed in small and/or intermediate-sized cells. Large neurons only contained CGRP, VIP, NPY, beta-END, ENK, and GABA. The percentage of immunostained neurons varied for the various antisera: less than 10% of cultured neurons were positive for ENK, beta-LPH, beta-END, DYN, VASO, and OXY; 10-30% for SOM, CCK, CAT, and SP; and greater than 30% for NPY, CRF, GLU, NT, VIP, GABA, GRP, CGRP, 5-HT, and TRH. In the latter two groups of transmitters (except CGRP), the proportion of immunoreactive neurons was by far larger in cultured than in freshly dissociated DRG. The most pronounced (greater than 25%) increase in the proportion of positively stained neurons after culturing was observed for the GRP, CRF, TRH, and 5-HT antisera. Serotonin was the only transmitter identified in cultured but not in freshly dissociated cells. These data indicate, on one hand, that various antigens, for example, CAT, GABA, NT, TRH, NPY, beta-LPH, and beta-END, which up to now have not been described in DRG in situ, can be detected immunocytochemically a few hours after dissociation of adult rat DRG. On the other hand, several transmitters, for example, VIP, NPY, SP, GABA, GLU, NT, GRP, CRF, TRH, and 5-HT, are expressed in a significantly higher proportion of cells in cultured than in freshly dissociated preparations. This might reflect a change in the phenotypic expression of transmitters due to the new environment generated by the culture conditions, a hypothesis that can be tested by measuring specific mRNA levels. Moreover, considering the plasticity and multipotentiality of their transmitter phenotype, cultured adult DRG neurons might represent an interesting material for autografts into the injured central nervous system.
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PMID:Neurotransmitter phenotype plasticity in cultured dissociated adult rat dorsal root ganglia: an immunocytochemical study. 256 40

In an attempt to characterize GH and PRL secretion in acromegaly, the effects of various stimuli on GH and PRL release by cultured pituitary adenoma cells derived from acromegalic patients were studied. In addition, the PRL responses of somatotroph adenoma cells were compared to those of prolactinoma cells. GH-releasing hormone-(1-44) (GHRH) consistently stimulated GH secretion in all 14 somatotroph adenomas studied in a dose-dependent manner. The sensitivity as well as the magnitude of the GH responses to GHRH were highly variable in individual tissues. Somatotroph adenomas that did not respond to dopamine were more sensitive and had greater GH responses to GHRH. In 8 of 9 somatotroph adenomas that concomitantly secreted PRL, the addition of GHRH likewise increased PRL release. Omission of extracellular Ca2+ blocked the stimulatory effect of GHRH on GH and PRL secretion. When cells were coincubated with 0.1 nM somatostatin, GH and PRL secretion induced by 10 nM GHRH were completely blocked in most adenomas. Similarly, coincubation of dopamine resulted in inhibition of GHRH-induced hormone secretion in some adenomas. Addition of TRH to the incubation medium, on the other hand, significantly stimulated GH secretion in 8 of 14 adenomas, while TRH stimulated PRL release in all of the adenomas. Vasoactive intestinal peptide (VIP) and corticotropin-releasing hormone (CRH) produced an increase in GH and PRL secretion in other adenomas. In prolactinoma cells, somatostatin and dopamine unequivocally suppressed PRL secretion; however, other stimuli including GHRH, VIP, and CRF were ineffective. TRH induced a significant increase in PRL secretion in only one prolactinoma. These results suggest that responsiveness to GHRH and somatostatin is preserved in somatotroph adenomas; the responsiveness to GHRH is inversely correlated to that to dopamine; and PRL cells associated with somatotroph adenomas possess characteristics similar to those of GH cells. Further, the GH stimulatory actions of TRH and VIP are different.
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PMID:Effects of hypophysiotropic factors on growth hormone and prolactin secretion from somatotroph adenomas in culture. 285 94


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