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 oligopeptides were microiontophoretically applied to neurons of the sensory cortex, hippocampus, thalamus and septum. Metenkephalin and beta-endorphin increased activity of some neurons while decreasing it in other cells. Nalorphine antagonized the inhibition effect of metenkephalin in all the brain areas under study. Inhibition of the peptide activating action occurred in hippocampal and septal neurons. A correlation between effects of metenkephalin and beta-endorphin on the same neurons was revealed in the cortex and thalamus. Thyroliberin mostly activated neurons in all the areas. Independence of neuronal effects of TRH and opioid peptides was obvious.
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PMID:[Sensitivity of neurons in different regions of the brain to met-enkephalin, beta-endorphin, and thyroliberin in the rat]. 626 11

Radiofrequency lesions of either the dorsal (LD) or the median (LM) raphe nuclei of male rat mesencephalon did not modify baseline levels of plasma prolactin (PRL). However, the PRL releasing effect of 30 min of immobilization stress was suppressed in LM rats and enhanced in LD rats. The PRL releasing effect of pentobarbital (PB, 50 mg/kg, IP) or of beta-endorphin (END, 15 micrograms/rat, intracerebroventricularly, ICV) also was enhanced in LD rats. TRH (10 micrograms/rat, ICV) administered concomitantly with either PB or END, antagonized the releasing effect of the former and enhanced the releasing effect of the latter in sham operated rats. Lesions of the raphe nuclei blocked the antagonizing effect of TRH, while the enhancing effect was heightened in LD rats. These results indicate that neurons originating in the raphe nuclei are not involved in the control of baseline plasma PRL levels. They indicate, furthermore, the existence of an inhibitory pathway originating in the dorsal raphe nucleus the suppression or activation of which is, at least partly, the mechanism of PB, END or TRH effects on PRL release. The PRL releasing effect of immobilization stress seems to be under a dual, mutually antagonistic control: activating through the median and inhibitory through the dorsal nucleus.
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PMID:Role of midbrain raphe nuclei in stress-, pentobarbital-, beta-endorphin-, or TRH-induced changes in plasma PRL levels of adult male rats. 627 49

Most neuropeptides are known to occur both in the central nervous system and in blood. This, as well as the occurrence of central nervous peptide effects after peripheral administration, show the importance of studying the relationships between the peptides in the two compartments. For many peptides, such as the enkephalins, TRH, somatostatin and MIF-1, poor penetration of the blood-brain barrier was shown. In other cases, including beta-endorphin and angiotensin, peptides are rapidly degraded during or just after their entry into brain or cerebrospinal fluid. Some peptides, such as insulin, delta-sleep-inducing peptide, and the lipotropin-derived peptides, enter the cerebrospinal fluid to a slight or moderate extent in the intact form. Many peptide hormones, such as insulin, calcitonin and angiotensin, act directly on receptors in the circumventricular organs, where the blood-brain barrier is absent. Oxytocin, vasopressin, MSH, and an MSH-analog alter the properties of the blood-brain barrier, which may result in altered nutritient supply to the brain. In conclusion, the diffusion of most peptides across the brain vascular endothelium seems to be severely restricted. There are, however, several alternative routes for peripheral peptides to act on the central nervous system. The blood-brain barrier is a major obstacle for the development of pharmaceutically useful peptides, as in the case of synthetic enkephalin-analogs.
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PMID:Minireview. Peptides and the blood-brain barrier. 630 42

Naloxone has been used as a pharmacological tool to investigate the role of endorphins and opiate receptors in the cardiovascular pathophysiology of shock. It would appear that endorphins act on opiate receptors to contribute to the abnormalities found and that naloxone improves survival as well as cardiovascular function in shock. Preliminary studies in humans and the subhuman primate create cautious optimism regarding the clinical application of this information. Naloxone has served us well as a key to unlock the involvement of endorphins and opiate receptors in shock. However, further advances in our understanding may depend on the development and use of opiate receptor agonists and antagonists specific for the different opiate receptors described, each subserving different functions. Naloxone's disadvantage of increasing pain awareness may limit its clinical usefulness but might be overcome by using drugs that reverse the behavioral and neuroendocrine changes produced by beta-endorphin without altering pain relief. Thyrotropin-releasing hormone (TRH) is just such a "physiological" opiate antagonist which has been shown to increase MAP in experimental endotoxic and hemorrhagic shock [32].
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PMID:Naloxone in endotoxic shock: experimental models and clinical perspective. 630 74

Clinical and biochemical findings in 13 patients (11 women and 2 men) with macronodular adrenocortical hyperplasia (MNH; nodule size, greater than 0.5 to 5.3 cm) were compared with those of 18 patients (15 women and 3 men) with Cushing's disease and diffuse (n = 9) or micronodular (n = 9) hyperplasia (DH). All were bilaterally adrenalectomized for their hypercorticism. The clinical picture was almost identical in both groups, except for greater frequency of hypertension (13 of 13 vs. 10 of 18; P less than 0.05), alopecia (4 of 11 vs. 0 of 15; P less than 0.05), and scintigraphic lateralization (6 of 7 vs. 1 of 7; P less than 0.05) in the MNH group than in the DH group. The sella turcica was enlarged in 30% of the patients in both groups. Patients with MNH were significantly older than DH patients [43.5 +/- 7.8 (mean +/- SD) vs. 31.7 +/- 10.1 yr; P less than 0.005] and had a 3-fold longer duration of disease (7.8 +/- 4.6 vs. 2.0 +/- 1.1 yr; P less than 0.001) than those with DH. The mean plasma ACTH and cortisol levels and urinary 17-hydroxycorticosteroid excretion were elevated in both MNH and DH patients and responded similarly to specific (corticotropin-releasing hormone and metyrapone) and nonspecific (TRH and LHRH) stimuli. However, dexamethasone suppressibility and the stimulatory effect of ACTH on adrenocortical function were less in the MNH than in the DH group or its subgroups, suggesting a greater degree of adrenal autonomy in the former. Adrenal weight in MNH (15.8 +/- 12.1 g each) was almost twice as high as in DH (8.2 +/- 2.0 g) patients and positively correlated with the duration of the disease. The data suggest that MNH may be a result of long-standing Cushing's disease with varying degrees of pituitary dependence and adrenocortical autonomy, which may lead to confusing biochemical and radiological findings. Bilateral adrenalectomy, rather than hypophysectomy, is the treatment of choice in MNH.
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PMID:Macronodular adrenocortical hyperplasia in long-standing Cushing's disease. 631 61

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 investigate whether TRH could be an important PRL-releasing factor during suckling in the rat. Plasma PRL, TSH, beta-endorphin-like immunoreactivity, and GH responses in serial blood samples from unanesthetized suckled rats were determined. The resulting hormonal profile was compared with that obtained when TRH (500 ng/kg BW, iv) was injected at the onset of suckling. Suckling evoked a rise in plasma levels of PRL, beta-endorphin-like immunoreactivity, and GH, but not in TSH. In contrast, exogenous TRH caused a 9-fold increase in plasma TSH levels during suckling without further increasing the PRL response. Since plasma PRL responses are reportedly enhanced by previous suckling, we also determined plasma PRL and TSH levels when TRH (25 ng/rat, iv) was given 30 min after a brief suckling episode. TRH caused a 2.5-fold increase in plasma TSH, but did not significantly increase plasma PRL levels. Since suckling increases plasma PRL without increasing plasma TSH, and TRH increases TSH but not PRL levels, we conclude that TRH is not a major PRL-releasing factor during suckling.
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PMID:Evidence that thyrotropin-releasing hormone is not a major prolactin-releasing factor during suckling in the rat. 632 54

Thyrotropin-releasing hormone (TRH) stimulates alpha-melanocyte-stimulating hormone (alpha-MSH) secretion in amphibia as well as thyrotropin-stimulating hormone (TSH) and prolactin secretions in mammals. Since thyroid hormones regulate the stimulatory effect of TRH on TSH and prolactin, the possible role of thyroxine (T4) in the control of alpha-MSH secretion in amphibia, has been investigated. Neurointermediate lobes of Rana ridibunda were perifused in amphibian culture medium for 7 hr and the amounts of alpha-MSH released into the effluent perfusate were measured by radioimmunoassay. In vivo treatment with T4 (0.5 mg/kg twice a day for 9 days) did not modify the in vitro response of the neurointermediate lobes to TRH (10(-9) to 10(-7) M). In addition, prolonged infusion of T4 in vitro did not alter spontaneous and TRH-induced alpha-MSH release. In spite of the inhibitory effect of T4 on TRH-induced TSH and prolactin secretions in mammals, the present data show that, in frogs, thyroid hormone does not modulate the stimulation of alpha-MSH secretion induced by TSH.
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PMID:In vitro study of frog (Rana ridibunda Pallas) neurointermediate lobe secretion by use of a simplified perifusion system. II. Lack of action of thyroxine on TRH-induced alpha-MSH secretion. 641 78

Serum LH, FSH, TSH, PRL, GH and cortisol levels were measured in 10 patients with a craniopharyngioma both before and after a combined insulin-induced hypoglycaemia, GnRH and TRH test. In pre-operative studies, only two patients did not show hormonal abnormalities, while eight patients had deficiencies of one or more hormones. The most frequent abnormality was GH deficiency (six cases), followed by gonadotropin (four cases), cortisol (four cases), and TSH (one case), whereas four patients showed high serum PRL values. In post-surgical studies, a significant improvement of pituitary function was observed in two cases, whereas an impairment of previously normal corticotropin reserve was recorded in another case. The data obtained suggest that endocrine abnormalities in patients with craniopharyngiomas are irreversible in most cases.
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PMID:Evaluation of anterior pituitary function in adult patients with craniopharyngiomas. 643 39

A new clonal strain of Prl-secreting cells derived from the transplantable rat pituitary tumour, 7315a, has been established in culture. The cells of this strain, designed 235-1, have a highly developed Golgi complex, an extensive rough endoplasmic reticulum, and a few small but no large dense-core granules. When inoculated into athymic mice and rats of the Buffalo strain, the 235-1 cells produce tumours, and the host animals have hypertrophied mammary glands that produce milk, indicating that Prl secreted by these cells has mammotrophic activity. In monolayer culture, the doubling time of 235-1 cells is 31 +/- 1 h (mean +/- SE). The cells secrete Prl, a trace quantity of GH, but no LH, FSH, TSH, ACTH, or alpha-MSH. Prl is released at a rate of 257 +/- 12 fg per h per cell. The cellular content of Prl is 424 +/- 23 fg per cell. Prl secretion by 235-1 cells is not affected by dopaminergic agonists and antagonists, TRH, or oestradiol-17 beta but is inhibited in the presence of EGTA or monensin, an ionophore that is believed to act at the level of the Golgi complex. The subcellular distribution of Prl in 235-1 cells is different from that in rat pituitary cells. In 235-1 cells, Prl is associated not with a single set of dense particles as it is in pituitary cells but with 2 sets of subcellular particles, of which 1 set cosedimented with particles having lysosomal enzyme activity. These findings suggest that Prl secretion by 235-1 cells involves secretory pathways that are different from those seen in normal lactotrophs.
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PMID:A new clonal strain of rat pituitary tumour cells: a model for non-regulated secretion of prolactin. 643 12


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