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 ability of hormones to bind to their functional receptors on turtle (Pseudemys scripta) endocrine target tissues in the cold was tested by treating tissues with secretagogues at low temperatures (5-15 degrees) and then following subsequent target stimulation in the absence of secretagogue at a warm temperature (28 degrees). Administration of thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone, and growth hormone-releasing hormone to pituitaries at low temperatures (20 degrees or below) suppressed responses in growth hormone (GH) and thyrotropin (TSH) secretion and there was little or no response in pituitaries subsequent to warming. In contrast, gonadotropin-releasing hormone treatment of pituitaries, TSH treatment of thyroid glands, and gonadotropin (FSH and LH) treatment of testes in the cold (down to 5 degrees) was followed by a large response in the target glands (secretion of LH, thyroxine, and testosterone (T), respectively) following warming. Additional studies with FSH and LH showed that these hormones can bind to testes rapidly (within 5 min) at low temperatures where no acute response is observed, although the dose sensitivity and the extent of this priming in the cold are less than at warm temperatures. Thus, postreceptor events may be more important than binding per se for temperature effects on hormone responses of tissues, but even this component of cell function varies among tissues. The effects of a receptor-independent secretagogue (tetraethylammonium chloride), which causes cell depolarization by blocking K+ efflux, were also blocked at low temperatures in thyrotropes and somatotropes but not in gonadotropes. Rapid depressions in TSH and GH secretions following cooling of TRH-stimulated pituitaries and of T secretion in LH-stimulated testes provide further evidence for cold sensitivity of postreceptor processes in these tissues.
Gen Comp Endocrinol 1990 Dec
PMID:The role of hormone binding in the cold suppression of hormone stimulation of the pituitary, thyroid, and testis of the turtle. 228 80

Plasma levels of the N-terminal peptide of proopiomelanocortin (NPP) were measured in rainbow trout, Salmo gairdneri, following treatment of handling stress with or without administration of dexamethasone, adaptation to white and black background, and maintenance on a constant light/dark cycle. Effects of exogenously administered NPP on plasma constituents were also examined to provide insight into the biological significance of NPP. Thirty minutes of handling stress in shallow water had no effect on plasma levels of NPP during and after the stress period, whereas significant increases in plasma cortisol and glucose were observed. Intraperitoneal administration of dexamethasone blocked the stress-induced elevation of plasma levels of cortisol and caused a depression of plasma NPP. No difference was observed in plasma levels of NPP between trout adapted to a white background and those adapted to a black background. No diurnal changes in NPP were observed under an artificial light/dark cycle (14L/10D light cycle, 0500-1900 hr light) in May and September. Thus, plasma levels of NPP were considerably constant under various physiological conditions, and no synchronism was observed between plasma NPP and cortisol, although NPP modifies the corticotropin-induced release of cortisol from the interrenal. Plasma constituents such as cortisol, total protein, albumin, plasma amino nitrogen, glucose, free fatty acid, ketone body, sodium, potassium, calcium, and magnesium were not altered by intraperitoneal injections of NPP (1 or 10 micrograms) once daily for 6 days (total of six injections) or once every other day for 28 days (14 injections). High concentrations of NPP were found in the plasma 24 hr after cessation of the serial injections of NPP (10 micrograms), suggesting slow metabolic clearance of the peptide.
Gen Comp Endocrinol 1990 Jan
PMID:Plasma profiles of the N-terminal peptide of proopiomelanocortin in the rainbow trout with reference to stress. 229 28

Light microscopic double immunocytochemical stainings, performed on sea bass hypothalamo-hypophysial sections, revealed the projection of different neuropeptide-immunoreactive neurons innervating the hormone-producing cell populations in the pituitary gland. In the rostral pars distalis (PD) the ACTH cells were found in close proximity to fibers immunoreactive for somatostatin (SRIF), growth hormone-releasing hormone (GRF), corticotropin-releasing hormone (CRF), vasotocin (VT), isotocin (IT), substance P (SP), neurotensin, and galanin (GAL), while the PRL cell zone seemed only innervated by nerve fibers immunopositive for GAL. In the proximal PD, fibers immunoreactive for SRIF, GRF, VT, IT, cholecystokinin, SP, neuropeptide Y, and GAL formed a close relationship with the growth hormone cells. The gonadotrophs were observed near nerve fibers immunostained for gonadotropin-releasing hormone, IT, and less obviously GRF and VT, while fibers positive for GRF, CRF, VT, IT, SP, and GAL penetrated between and formed a close association with the thyrotrophs. In the pars intermedia the MSH cells and the PAS-positive (PAS+) cells seemed both innervated by separate nerve fibers immunoreactive for GRF, CRF, melanin concentrating hormone, VT, IT, and SP. All these results suggest a functional role of the neuropeptides in the adenohypophysis of the sea bass, possibly in the synthesis and/or release of hypophysial hormones from the different cell types.
Gen Comp Endocrinol 1989 Feb
PMID:Immunocytochemical demonstration of close relationships between neuropeptidergic nerve fibers and hormone-producing cell types in the adenohypophysis of the sea bass (Dicentrarchus labrax). 246 54

To assess central nervous system cholinergic neuroendocrine regulation in Alzheimer's disease (AD), we measured plasma arginine vasopressin, beta-endorphin, and epinephrine responses to a cholinergic challenge elicited by intravenous administration of the acetylcholinesterase inhibitor physostigmine (0.0125 mg/kg) in male patients with AD (n = 12) and compared their responses with those of age-matched normal control subjects (n = 12). Physostigmine promptly increased plasma arginine vasopressin (tenfold), beta-endorphin (twofold to threefold) and epinephrine (threefold) levels in elderly control subjects. In contrast, patients with AD showed attenuated responses to physostigmine. When controls and patients with AD who experienced nausea (n = 2 and n = 6, respectively) were excluded, the arginine vasopressin, beta-endorphin, and epinephrine responses of patients with AD were significantly less than those of control subjects. These data suggest that the central nervous system cholinergic deterioration of AD results in decreased responsiveness of neuroendocrine systems that are regulated by central cholinergic mechanisms.
Arch Gen Psychiatry 1989 Jun
PMID:Neuroendocrine responses to physostigmine in Alzheimer's disease. 252 15

The purpose of the present investigation was to examine the receptor specificity of dopamine inhibition of gonadotropin (GtH) and alpha-melanocyte-stimulating hormone (alpha-MSH) release from the goldfish (Carassius auratus) pituitary in vitro. Pars distalis (PD) and neurointermediate lobe (NIL) fragments of the goldfish pituitary were superfused in vitro under various experimental paradigms; eluate from PD and NIL fragments was analyzed for (GtH) and (alpha-MSH), respectively. Spontaneous GtH release from PD fragments was relatively constant over 6 hr; continuous superfusion with dopamine reversibly inhibited spontaneous GtH release with an estimated ED50 of 10(-4.4) M. Domperidone, a specific D-2 receptor antagonist, reversed the inhibitory action of dopamine and increased spontaneous GtH release. Acute treatment of PD fragments with salmon GnRH (sGnRH) stimulated GtH release; dopamine inhibited GtH release from similarly treated fragments with an ED50 of 10(-7.5) M. The spontaneous release of alpha-MSH from NIL fragments was relatively constant over 6 hr; continuous superfusion with dopamine reversibly inhibited this release with an ED50 of 10(-7.2) M. Acute treatment of NIL fragments with thyrotropin-releasing hormone (TRH) caused acute dose-related increases in alpha-MSH release with an ED50 of 10(-8.2) M; dopamine reversibly inhibited alpha-MSH release from similarly treated fragments with an ED50 of 10(-7.7) M. Both stereoisomers of apomorphine, a dopamine agonist, inhibited GtH release from PD fragments treated with sGnRH; in contrast, alpha-MSH release from NIL fragments treated with TRH was stereospecifically inhibited by (-)-apomorphine, but not by (+)-apomorphine. Domperidone reversed (ED50 = 10(-6.6) M) dopamine (10(-6.3) M) inhibition of GtH release from PD fragments treated with sGnRH. In NIL fragments, the inhibitory action of dopamine (10(-6.3) M) was reversed by domperidone (ED50 = 10(-5.5) M), which restored the acute alpha-MSH release response to TRH. These results suggest the involvement of a low-affinity dopamine/neuroleptic receptor in dopamine inhibition of GtH and alpha-MSH release from the pituitary of the goldfish.
Gen Comp Endocrinol 1989 Jun
PMID:Dopamine inhibition of gonadotropin and alpha-melanocyte-stimulating hormone release in vitro from the pituitary of the goldfish (Carassius auratus). 252 42

1. The antinociceptive effect of compound 48/80 was reversed by the pretreatment with an angiotensin-converting enzyme (ACE) inhibitor, Hoe 498, in a dose-dependent manner and with a opiate receptor antagonist, naloxone (5.0 mg/kg, s.c.) in rats. 2. The increase of plasma beta-endorphin-like immunoreactivity produced through s.c. administration of compound 48/80 was attenuated by the pretreatment with Hoe 498 but not with naloxone. 3. The present data suggest the possible involvement of renin-angiotensin system in compound 48/80-induced analgesia in rats.
Gen Pharmacol 1989
PMID:The role of renin-angiotensin system in compound 48/80-induced analgesia in rats. 252 74

1. Connective tissue massage produces relief of pain and increases microcirculation in a number of vascular beds. 2. The concentration of plasma beta-endorphins has been measured in 12 volunteers before and 5, 30 and 90 min after a 30-min session of connective tissue massage. 3. There was a moderate mean increase of 16% in beta-endorphin levels from 20.0 to 23.2 pg/0.1 ml (P = 0.025), lasting for about 1 hr with a maximum in the test 5 min after termination of the massage. 4. It is assumed that the release of beta-endorphins is linked with the pain relief and feeling of warmth and well-being associated with the treatment.
Gen Pharmacol 1989
PMID:Increase of plasma beta-endorphins in connective tissue massage. 252 75

In the present study, we have localized for the first time beta-endorphin (beta-EP)-like material in the adult and larval urodele and anuran tissues using immunohistochemical techniques. In the adult Notophthalmus viridescens and Ambystoma mexicanum, strong immunoreactivity to beta-EP antisera was observed in the region of the intermediate lobe, the latter fluorescing as a discrete body. The fluorescence was confined to the periphery of the cells, while the nuclei and the immediately surrounding cytoplasmic regions of the cells remained unstained. A few scattered cells in the anterior pituitary gland as well as the tracts in the posterior lobe also exhibited positive staining, although not as strong as the intermediate lobe. In the larval urodele, A. maculatum, beta-EP-like material was localized for the first time in the sensory ganglia and their emerging nerve fibers, in the Leydig cells of the skin, as well as in a few discrete cells scattered among stomach epithelial cells. In addition to the above, immunoreactivity to beta-EP antisera was observed in the cellular intermediate part of the neurointermediate lobe of the pituitary gland in young Xenopus laevis, the neural part of the lobe remaining nonreactive.
Gen Comp Endocrinol 1989 Aug
PMID:Immunohistochemical localization of beta-endorphin-like material in the urodele and anuran amphibian tissues. 253 Jan 30

To explore the relationship of central and peripheral adrenocorticotropic hormone (ACTH, or corticotropin) levels to hypothalamo-pituitary-adrenal axis dysfunction in patients with eating disorders, levels of cerebrospinal fluid (CSF) and plasma ACTH, cortisol, and 24-hour urinary free cortisol were measured in 16 patients with anorexia nervosa (60% +/- 1.1% of ideal body weight), 14 patients with bulimia (93.2% +/- 4.6% of ideal body weight), and 11 healthy age-matched women volunteers. The CSF, plasma, and urinary free cortisol levels were elevated in underweight anorexic patients and showed declines following weight recovery. Cortisol-binding globulin levels were similar in anorexics and controls. In contrast, underweight anorexics showed low CSF ACTH levels that returned to normal following weight recovery, and their plasma ACTH levels were normal. On hospital admission, bulimic patients demonstrated normal ACTH and cortisol levels. After their abstinence from binge-purge episodes, the CSF ACTH levels decreased significantly. Positive relationships were found among CSF, plasma, and urinary cortisol levels, and inverse relationships were seen between cortisol measures and CSF ACTH levels in patients with eating disorders. Secretion of ACTH into the CSF may respond to feedback by cortisol or, alternatively, may be suppressed by the hypersecretion of corticotropin-releasing hormone, leading to the depletion of the pro-opiomelanocortin molecule.
Arch Gen Psychiatry 1989 Jan
PMID:Central and peripheral ACTH and cortisol levels in anorexia nervosa and bulimia. 253 25

alpha-Melanotropin (alpha-melanocyte-stimulating hormone, alpha-MSH) is a tridecapeptide, Ac-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2. The minimal sequence of alpha-MSH required for agonism in the lizard (Anolis carolinensis) skin bioassay was determined to be Ac-His-Phe-Arg-Trp-NH2 (Ac-alpha-MSH6-9-NH2). Smaller fragments of this sequence (Ac-alpha-MSH6-8-NH2, Ac-alpha-MSH6-7-NH2, Ac-alpha-MSH7-9-NH2, and Ac-alpha-MSH7-8-NH2) were devoid of melanotropic activity. The tetrapeptide, Ac-alpha-MSH7-10-NH2, was also inactive, thus again demonstrating the importance of His at position 6 for minimal activity. The important potentiating amino acids were found to be Met-4, Lys-11, and Pro-12, since Ac-alpha-MSH4-10-NH2 was about 100 times more potent than Ac-alpha-MSH5-10-NH2, and Ac-[Nle4]-alpha-MSH4-11-NH2 was about 40 times more potent than Ac-alpha-MSH4-10-NH2 or Ac-[Nle4]-alpha-MSH4-10-NH2. Ac-alpha-MSH4-12-NH2 and Ac-[Nle4]-alpha-MSH4-12-NH2 were equipotent and about six times more potent than alpha-MSH. Since [Nle4]-alpha-MSH and Ac-[Nle4]-alpha-MSH4-13-NH2 were both equipotent but about sixfold less active than Ac-[Nle4]-alpha-MSH4-12-NH2, it is clear that valine at position 13 does not contribute to the potency of alpha-MSH, except possibly in a negative way. The minimal message sequence for equipotency to alpha-MSH appears to be Ac-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-NH2, since the analog, Ac-[Nle4]-alpha-MSH4-11-NH2, was as active as the native hormone. Ser-1, Tyr-2, Ser-3, Glu-5, and Val-13 are not important for melanotropic potency since Ac-alpha-MSH4-12-NH2 was more potent than alpha-MSH, and Ac-alpha-MSH5-10-NH2 and Ac-alpha-MSH6-10-NH2 were equipotent, being about 4,000 times less active than alpha-MSH.
Gen Comp Endocrinol 1989 Jan
PMID:Alpha-melanotropin: the minimal active sequence in the lizard skin bioassay. 253 78


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