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)

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

Effects of thyrotropin-releasing hormone (TRH) on the plasma beta-endorphin-like immunoreactivity (beta-Ep-LI) levels in rats have been studied. TRH (10 mg/kg) were injected i.v., and the animals were serially decapitated. The plasma beta-Ep-LI levels were measured by radioimmunoassay. Effects of TRH on beta-Ep-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-Ep-LI content in the hypothalamus, pituitary gland or adrenal gland did not change significantly after TRH injection. The plasma beta-Ep-LI levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. In the hypophysectomized rats, the plasma beta-Ep-LI levels were lower than that of the control, and did not change significantly after TRH injection. beta-Ep-LI release from anterior pituitary in vitro significantly decreased after the addition of TRH to medium. These findings suggest that TRH may act on the pituitary gland to reduce plasma beta-Ep-LI levels in rats.
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PMID:Thyrotropin-releasing hormone reduces the plasma levels of beta-endorphin-like immunoreactivity in rats. 295 35

The course of plasma beta-endorphin/beta-lipotropin, cortisol and prolactin (PRL) levels was followed from 0.5 till 5 h after normal delivery in 13 healthy women. Six subjects who did not want to breast-feed their child received 2.5 mg bromocriptine orally 1 h after delivery. After 3 h the effect of the intravenous administration of 200 micrograms thyrotropin-releasing hormone (TRH) was also measured. Elevated plasma beta-endorphin and cortisol levels decreased after delivery in a (log) linear fashion which was not influenced by bromocriptine. TRH elicited a significant short-lived identical increase in plasma beta-endorphin/beta-lipotropin concentrations in the control and the bromocriptine-treated subjects. TRH similarly delayed the rapid decline in plasma cortisol levels in both groups of women. Basal and TRH-induced PRL levels were rapidly suppressed by bromocriptine. These studies show the presence of a paradoxical increase of beta-endorphin/beta-lipotropin and cortisol levels in response to TRH occurring shortly after delivery in normal women. This response cannot be mediated by the placenta. The absence of an inhibiting effect of bromocriptine on basal and TRH-induced beta-endorphin and cortisol release does not lend support to the hypothesis of the presence of a functionally active intermediate pituitary lobe in man early in puerperium.
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PMID:Bromocriptine is unable to suppress TRH-stimulated beta-endorphin/beta-lipotropin and cortisol secretion in normal pregnant women after delivery. 296 90

The neuroendocrine function is regulated by several neurotransmitters (acetylcholine, dopamine, somatostatin and noradrenaline) known to be reduced in brains of patients with Alzheimer's disease (AD). Moreover, the hypothalamus also has pathological changes. In spite of these findings suggesting neuroendocrine dysfunctions, this function has seldom been investigated in AD patients so far. We have compared patients with clinically 'probable' AD of mild-to-moderate severity with nondemented age- and sex-matched controls. Plasma levels of prolactin (PRL), growth hormone (GH) and thyroid-stimulating hormone (TSH) were measured by commercially available radioimmunoassays (RIA) before and after stimulation with metoclopramide, l-dopa or thyrotropin-releasing hormone. Basal plasma levels of beta-endorphin and beta-lipotropin were measured by RIA after high-performances liquid chromatography. Basal and stimulated plasma levels of PRL, GH, TSH and beta-lipotropin were similar in the two groups. Basal lamina levels of beta-endorphin were significantly higher in the patient group. Of doubtful clinical importance, this might be attributed to decreased tuberoinfundibular dopaminergic activity and has also been seen in patients with Parkinson's disease.
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PMID:Neuroendocrinological function in Alzheimer's disease. 297 29

Ovine corticotropin-releasing factor (oCRF) stimulates increased plasma immunoreactive adrenocorticotropin (IR-ACTH) and IR-cortisol at threshold, half-maximal, and maximal doses of 0.01-0.03, 0.3-1, and 3-10 micrograms/kg, respectively. Side effects occur with increasing frequency, severity, and duration at doses above 1 microgram/kg. oCRF has a prolonged duration of action, at least in part because of the long circulating half-life of intact oCRF in plasma. Increasing doses of oCRF given in late afternoon progressively diminish the next morning's circadian rise in plasma IR-ACTH in normal subjects, but not in Addisonian patients or subjects receiving metyrapone, indicating that prolonged oCRF-induced hypercortisolemia is the cause. Plasma IR-lipotropins and IR-beta-endorphin rise and fall concomitantly with IR-ACTH after oCRF injection. Arginine vasopressin increases the IR-ACTH response to oCRF fourfold when given simultaneously with oCRF. Cushing's disease patients respond variably, suggesting that oCRF may not be a very useful diagnostic agent in Cushing's syndrome. However, the combination of oCRF with growth hormone-releasing factor, gonadotropin-releasing hormone, and thyrotropin-releasing hormone appears to provide a rapid and useful test of combined anterior pituitary function.
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PMID:Clinical studies with synthetic ovine corticotropin-releasing factor. 298 41

Neuropeptides and biogenic amines known to be present in neurons or afferent terminals in the paraventricular nucleus (PVH), supraoptic nucleus (SON) and/or lateral hypothalamus (LH) were added to small areas of these structures obtained by micropuncture and cyclic adenosine monophosphate (cAMP) levels were measured. cAMP accumulation occurred in PVH, SON and LH in response to neuropeptides of the secretin family, such as vasoactive intestinal peptide (VIP) and in response to catecholamines. Bradykinin, alpha-melanocyte-stimulating (alpha-MSH), luteinizing hormone-releasing hormone (LH-RH), oxytocin and carbamylcholine stimulated cAMP accumulation selectively in one or two of the above structures. Glucagon, cholecystokinin (CCK), somatostatin (SRIF), corticotropin-releasing factor (CRF), thyrotropin-releasing hormone (TRH), adrenocorticotropin (ACTH), melanocyte-stimulating hormone (MSH), methionine enkephalin (Met-Enk), beta-endorphin, neurotensin, bombesin and angiotensin II did not effect cAMP levels while leucine enkephalin (Leu-Enk), arginine vasopressin and gamma-aminobutyric acid (GABA) elicited regionally selective decreases in basal levels of cAMP. When interactions between some of these compounds were measured, VIP and norepinephrine exerted a more than additive effect on cAMP elevation in the PVH, while the effect on cAMP of the SON and LH was additive.
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PMID:Interaction of neuropeptides and biogenic amines on cyclic adenosine monophosphate accumulation in hypothalamic nuclei. 300 57

Twenty-two subjects (11 patients with major endogenous depression and 11 controls) received an intravenous test dose of 100 micrograms human corticotropin-releasing hormone (h-CRH). Corticotropin (ACTH), but not cortisol, responses were blunted in depressives. Basal cortisol secretion was higher in depressives than in controls and was negatively correlated to the corticotropin response following h-CRH. This finding indicates the integrity of the glucocorticoid-dependent negative feedback regulation in depression and supports the view that hypercortisolism in depression is primarily due to a suprapituitary disturbance. Comparison of ACTH responses after h-CRH with thyrotropin (TSH) output following thyrotropin-releasing hormone (TRH) revealed a positive correlation (r = 0.65, p less than 0.001). The concordance between ACTH and TSH responses after specific challenges suggests that regulation of both systems is at least in part under a common control.
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PMID:Human corticotropin-releasing hormone in depression--correlation with thyrotropin secretion following thyrotropin-releasing hormone. 301 Nov 29

In amphibians, alpha-MSH secretion is stimulated by thyrotropin-releasing hormone (TRH). In the present study we show that extracellular calcium influences directly the spontaneous secretion of alpha-MSH and that it participates in the mechanism of action of TRH on frog melanotrophs.
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PMID:[Role of calcium in TRH-induced secretion of alpha-MSH in the frog]. 309 25

Effects of growth hormone-releasing hormone (GRH) and corticotropin-releasing hormone (CRH) on the release of immunoreactive thyrotropin-releasing hormone (ir-TRH) from the rat hypothalamus in vitro were studied. The rat hypothalamus was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) for 20 min. The amount of ir-TRH release into the medium was measured by radioimmunoassay. The ir-TRH release from the rat hypothalamus was inhibited significantly in a dose-related manner with the addition of GRH or CRH. These findings suggest that GRH and CRH inhibit ir-TRH release from the rat hypothalamus in vitro.
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PMID:Effects of growth hormone-releasing hormone and corticotropin-releasing hormone on the release of thyrotropin-releasing hormone from the rat hypothalamus in vitro. 313 Nov 50

The present studies were carried out to investigate the mechanisms through which systemic angiotensin II (AII) acts within the central nervous system to influence the release of anterior pituitary hormones in the Sprague-Dawley rat. In particular, these studies have examined the role of the subfornical organ (SFO) as an essential structure mediating these responses. Extracellular single-unit recordings were obtained from 199 paraventricular nucleus (PVN) neurons antidromically identified as projecting to the median eminence. Different groups of these neurons were tested for the effects of either electrical stimulation in the SFO (n = 87) or systemic AII administration in intact (n = 49) and SFO-lesioned (n = 25) animals. Of cells tested with SFO stimulation 45% were excited, 16% inhibited, and the remainder unaffected. Neurons which were excited were primarily located just medial to the magnocellular neurons in the region where the majority of corticotropin-releasing hormone immunoreactive cells are found. In contrast, inhibitory responses were observed in cells located in the dorsal medial PVN, a region containing thyrotropin-releasing hormone, somatostatin, and dopamine PVN-median eminence neurons. Following systemic AII 42% of cells tested showed increased activity specific to the effects of this peptide, and 20% showed alterations in activity associated with the cardiovascular changes induced by AII. In contrast, following SFO lesion only 8% of neurons tested showed specific excitatory responses to AII. In order to test the hypothesis that systemic AII may activate this excitatory SFO to PVN pathway, a further group of 35 neurons were tested with both SFO stimulation and AII.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic angiotensin acts at the subfornical organ to control the activity of paraventricular nucleus neurons with identified projections to the median eminence. 339 33


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