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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present paper examines the role of pituitary pools of beta-endorphin in mediating the elevation in nociceptive threshold produced by stress. A 5 min foot-shock stress, characterized as activating both central and pituitary systems of beta-endorphin (beta-EP) and eliciting a naloxone-attenuated elevation in tail-flick latency in rats, was employed. Both total hypophysectomy and selective ablation of the anterior lobe almost completely abolished stress-induced analgesia (SIA), whereas removal of the neuro-intermediate lobe alone proved ineffective. However, manipulation of the hypothalamus-pituitary-adrenal feedback system by administration of either the corticosteroid, dexamethasone, or the corticosteroid synthesis inhibitor, metyrapone, in neither case affected SIA. None of these surgical or pharmacological manoeuvres affected basal nociceptive threshold (BNT). These data indicate that although the integrity of the adenohypophysis is essential for the manifestation of SIA, an adenohypophyseal mechanism, probably involving neither ACTH nor beta-EP, is essential for the development of the analgesia which accompanies stress.
Pain 1980 Jun
PMID:A non-beta-endorphinergic adenohypophyseal mechanism is essential for an analgetic response to stress. 625 Jan 16

Aging is associated with alterations in mood, thermoregulation, pain threshold, and stress response. Because these functions may be modulated by endogenous opiates, we measured immunoreactive ACTH with beta-endorphin in discrete brain areas and pituitary glands from rats aged 6 weeks (young), 6 months (mature), and 20-24 months (senscent). Beta-Endorphin and ACTH declined significantly with aging in the hypothalamus and corpus striatum. Beta-Endorphin and ACTH increased in the frontal lobe during early life; however, no change was noted after maturity. A discordant response with age was noted in the pituitary in that (ACTH did not change, while beta-endorphin increased early in life without change after maturity. Cerebellar tissue exhibited no immunoreactive ACTH or beta-endorphin. Age-related changes in brain and pituitary beta-endorphin and ACTH must be considered in the evaluation of the physiological aging process and when comparing studies of these neuropeptides.
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PMID:Age-related changes in central nervous system beta-endorphin and ACTH. 625 95

At the present time there is evidence for two families of related peptides which act as ligands for opiate receptor sites. The endorphin group of peptides are derived from the ACTH/LPH precursor pro-opiocortin. The enkephalins appear to be formed from a separate precursor or precursors that have yet to be fully characterized. There appear to be a number of different types of opiate receptors and this may be related to the multiplicity of peptide ligands that have so far been identified. The enkephalins and related peptides appear to have a much wider distribution than the endorphins but the latter may act as circulating hormones unlike the enkephalins. It is likely that both endorphins and enkephalins are involved in sensory modulation processes and release of these peptides has been demonstrated during brain stimulation for pain relief. The enkephalins are very rapidly inactivated by tissue proteases, the aminopeptidases appear largely responsible for the inactivation of exogenously administered enkephalins but the dipeptidyl carboxypeptidase, termed enkephalinase, may have a special inactivating function at enkephalinergic synapses. Evidence will be presented for the biosynthesis, the release and inactivation of the enkephalins relating to the above points.
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PMID:Opioid peptides: aspects of their origin, release and metabolism. 625 71

The knowledge of the amino acid sequence of both beta-lipotropin (beta-LPH) and gamma-LPH was the starting point that led to the hypothesis, considered revolutionary in 1967, that hormonal precursors exist. This concept was simultaneously proposed for proinsulin and applied later to other polypeptide hormones. The discovery of endorphins brought together two fields of research that were not related: the opiates and the so-called pituitary lipotropic hormones. The demonstration of specific brain opiate receptors led to the hypothesis of the existence of endogenous opiate ligands which could act as neurotransmittors. The isolation of such substances in the brain, first named enkephalins, revealed through their amino acid sequence their structural homology with the pituitary lipolytic hormones. The finding of a more potent opioid substance in the pituitary (beta-endorphin) that comprises the last 31 amino acids of beta-LPH shed a new light on the hypothesis proposed earlier which gave to beta-LPH a role as a precursor molecule. Finally, the addition of ACTH completed a putative multipotent precursor model that has been recently named pro-opiomelanocortin. Pulse-chase experiments have definitely proven that beta-endorphin is a maturation product of a large precursor also containing ACTH and MSH. In other studies, many groups have suggested that endorphins play important roles as possible neuromodulators in pain transmission, in analgesia, in tolerance and dependence, as well as on behavior and endocrine regulations, mainly those related to the hypothalamo-pituitary axes. The elucidation of the biosynthetic process or processes of cerebral endorphins (either enkephalins or beta-endorphin) is of primary importance in order ot understand better their biological as well as regulatory functions. These studies should also be applicable to the biosynthesis of all the other neuronal peptide hormones. It is hoped that they will provide new tools for the study of some important central nervous system functions, such as pain and endocrine control and the physiopathology of behavioral diseases.
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PMID:[Endorphins: structure, roles and biogenesis]. 626 34

A combination of radioimmunoassays and chromatography under acid-dissociating conditions has been used to obtain profiles of ACTH and LPH-related peptides in human plasma and cerebrospinal fluid. The spectra of peptides observed in these two fluids differ markedly. ACTH, beta-LPH, gamma-LPH and beta-endorphin are observed in the plasma of normal subjects and patients with increased pituitary ACTH secretion, whereas cerebrospinal fluid contains ACTH, beta-LPH, gamma-LPH and beta-endorphin, a 31 000-molecular-weight putative precursor having ACTH, LPH and gamma-MSH immunoreactivities, as well as pro-gamma-MSH(1-77) and smaller immunoreactive gamma-MSH fragments, alpha-MSH was not observed in blood or cerebrospinal fluid but this pars intermedia peptide and corticotropin-like intermediate lobe peptide (CLIP) were both found in tumour tissues obtained from patients with the ectopic ACTH syndrome. In vitro studies of human pituitary tumour tissues confirmed concomitant secretion of ACTH, beta-LPH, gamma-LPH, beta-endorphin and pro-gamma-MSH, which could be stimulated by a preparation of crude stalk median eminence and synthetic arginine vasopressin, from the rat, and could be suppressed by hydrocortisone. Clinical studies in which electroacupuncture was used to alleviate the symptoms of heroin withdrawal or recurrent pain revealed that concentrations of met-enkephalin and beta-endorphin, respectively, may rise in cerebrospinal fluid in association with relief of symptoms.
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PMID:Pars intermedia peptides: studies in adult humans. 626 79

In a clinical study we compared two groups of healthy patients at term: - 10 patients received no analgesics or very small doses of pethidine (control group) during the course of labour, - 17 patients were given CO2-bupivacaine via epidural catheter because they asked for it and because their obstetricians prescribed it (CEDA-group). After giving the same infusion solution of 120 ml/h 5% half-isotonic fructose to all the parturients, the following biochemical parameters were measured at the beginning and at the end of the first stage of labour, at delivery, and two hours later: Blood gases and acid-base status, blood sugar, lactate, betahydroxybutyric acid, ACTH, cortisol, hematocrit, electrolytes, and serum osmolality. The above mentioned parameters, except electrolytes and serum osmolality, were also determined in umbilical-cord blood immediately after delivery. In the labour ward, infants were observed and their capillary blood gases, acid-bases status, and blood sugar were measured 30, 60, and 120 minutes after birth. Lactate, betahydroxybutyric acid, ACTH, and cortisol levels rose significantly until delivery in both of the groups; significant differences between the two groups could be seen in blood gases, blood sugar, and ACTH levels. In the umbilical cord there were only significant differences in blood sugar. In summary it can be concluded that although labour pain can be controlled by epidural analgesia, the stress of labour is only influenced by different analgesic methods to a certain degree.
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PMID:[Important metabolic parameters in the peripartum period as affected by peridural anesthesia]. 626 40

The effects of neuroadenolysis on plasma titres of beta-endorphin, beta-lipotropin, ACTH, TSH and prolactin have been investigated in five patients with metastatic cancer who responded to the treatment and have been in remission for more than four years and in five others who were undergoing the treatment for the first time for pain due to cancer metastases. beta-Endorphin, beta-lipotropin and ACTH titres were within the normal ranges of values in both categories of patients but post-neuroadenolysis titres of these peptides were higher than those before the treatment. The ability to secrete TSH and prolactin and to respond to thyroid stimulating hormone releasing hormone (TRH) remains intact following the treatment. However, whereas basal TSH titres and response to TRH was lower in the majority of patients, no such effect was observed on prolactin secretion. Plasma titres of prolactin and TSH were below the sensitivity of the method in the five patients who are in remission for more than four years. These preliminary findings suggest that neuroadenolysis probably affects some mechanism(s) associated with the control of beta-endorphin, beta-lipotropin and ACTH synthesis.
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PMID:Some aspects of pituitary function after neuroadenolysis in patients with metastatic cancer. 627 71

In the rat compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The pain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotrophic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and G2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na+ and K+ by the nephron.
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PMID:[Influence of nutritional factors on the enhancement of renal compensatory hypertrophy by hyperadrenocorticism in the rat (author's transl)]. 627 45

beta-endorphin-like immunoreactivity was measured by radioimmunoassay in the brains of adult rats treated neonatally with beta-endorphin, naloxone, or vehicle. After treatment with beta-endorphin, the decreases observed in beta-endorphin-like immunoreactivity in the hypothalamus, pineal, midbrain, pons-medulla, hippocampus, striatum, frontal cortex, occipital cortex, and posterior cortex were highly significant but the 23% decrease in the thalamus was not significantly different from that of control rats. Neonatal administration of naloxone only resulted in a significant decrease in beta-endorphin-like immunoreactivity in the hypothalamus. In contrast, no differences were discernible in content of either beta-endorphin-like immunoreactivity or ACTH-like immunoreactivity in the pituitary of rats treated with beta-endorphin, naloxone, or vehicle in the neonatal period. These same rats had shown an increased threshold to painful thermal stimulation by the tail-flick test after administration of either beta-endorphin or naloxone at birth. The results suggest that neonatally injected beta-endorphin may alter the levels of beta-endorphin-like immunoreactivity in rat brain as well as the response to pain.
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PMID:Brain beta-endorphin-like immunoreactivity in adult rats given beta-endorphin neonatally. 627 60

The effect of large amounts of synthesized human beta-endorphin (beta-EP) administered intrathecally on pituitary-adrenocortical function was investigated by determining the plasma levels of ACTH, cortisol, growth hormone and prolactin in 8 patients with pain caused by severe disseminated cancer. They were divided into 2 groups, an Ep group of 8 patients and a control group of 5 of the same 8 patients. There were no significant effects of beta-Ep on plasma ACTH, cortisol and growth hormone levels. However, the injection of beta-Ep into human subjects resulted in a rise in plasma concentrations of prolactin.
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PMID:Effect of exogenous beta-endorphin on anterior pituitary hormone secretion in man. 627 26


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