Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Certain neuropeptides previously linked to stress and implicated in CNS control of analgesia/algesia were tested using a recently developed analgesiometric model, the rabbit ear-withdrawal test. The latency to ear withdrawal increased in a dose-related manner after beta-endorphin was injected intracerebroventricularly (IVC). Intermediate doses (0.5 and 1.0 micrograms) of adrenocorticotropic hormone (ACTH) caused hyperalgesia as indicated by decreases in latency. Corticotropin-releasing factor (CRF, 0.5 and 1.0 micrograms) also caused significant hyperalgesia late in the testing period. alpha-Melanocyte stimulating hormone (alpha-MSH, 0.25-2.0 micrograms), a molecule that shares the first 13 amino acid sequence with ACTH, and somatostatin (0.25-2.0 micrograms), caused no significant change in latency. However, 1.0 microgram doses of each peptide antagonized the analgesic effect of beta-endorphin (1.0 microgram) in the following order of potency: ACTH = alpha-MSH greater than CRF greater than somatostatin. The results support the idea that CNS peptides that are released during stress can exert opposing actions on acute pain, even though they may cause little effect alone.
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PMID:Influence of centrally administered peptides on ear withdrawal from heat in the rabbit. 288 94

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

beta-(Tyr9)melanotropin-(9-18), which itself has no analgesic action, as measured by the tail-flick and hot-plate methods, decreased morphine-induced analgesia following intracerebroventricular injection. H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH heptapeptide, which has weak CRF-like activity, had no action on analgesia and was not able to modify morphine-induced analgesia. Compared with ACTH1-24, which in a subcutaneous dose of 100 micrograms/rat decreased morphine-induced analgesia, the same dose of H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH was ineffective.
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PMID:The effects of beta-(Tyr9)melanotropin-(9-18) and H-Phe-Ile-Tyr-His-Ser-Tyr-Lys-OH on the analgesic action of morphine. 630 43

The experimental data clearly demonstrate that opioids (alkaloids as well as peptides) are able to inhibit nociception arising from inflamed tissue by a local peripheral action. mu- and delta- as well as kappa-opioid receptor ligands are effective by interaction with the respective opioid receptors presumably located in the terminal region of the sensory nerves. Similar effects are obtained when endogenous opioid peptides are released under stress conditions from immune cells present in the inflamed tissue. Immunoreactive beta-EP and enkephalins, processed in these cells, seem to be the relevant peptides in this respect. Although the mechanism of stress-induced release of opioid peptides from the immunocytes is presently not clear, there is indication that this process involves cytokines and CRF. Apart from immunological processes, inflammation-induced changes also take place at the level of the opioid receptors and are of significance in the manifestation of peripheral opioid antinociception; in particular the "activation" of these receptors apparently occurs at the early stages of inflammation when the infiltration of the tissue with immunocompetent cells is just beginning. There is increasing evidence for a therapeutic relevance of opioid-induced analgesia at peripheral sites of inflammation.
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PMID:Role of immune processes in peripheral opioid analgesia. 766 52

Amongst the spinal peptide candidates believed to be involved in the mediation of analgesia, only somatostatin fulfills the criterium of a real analgesia substance. Spinal somatostatin specifically blocks the transmission of painful stimuli. Spinal calcitonin may lower the opioid dose requirement in patients with bone metastases but it fails to relieve acute pain. The usefulness of ACTH and CRF for treatment of pain remains to be established. The role of CCK-8, vasopressin and neurotensin is unclear. The contradictory findings on antinociception using simple rodent withdrawal reflex tests (e.g. the tail flick test), or more complex behavioral tests in which supraspinal sensory processing is involved, (e.g. the hot plate test), indicate that these tests are inappropriate when neuropeptides are employed. Furthermore, due to their inability to predict analgesia in humans, they do not fulfill the guidelines proposed by the IASP that animal test procedures have to be for the benefit of humans.
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PMID:Non-opioid peptides for analgesia. 831 62

Our findings reviewed in this article have revealed that the stimulation of opioid receptors of the hypothalamic neurons by interferon alpha and beta-endorphin synthesized in the brain or by stress causing the opioid-dependent analgesia suppresses the natural killer cytotoxicity, an important component of immunosurveillance, through an activation of the hypothalamic CRF-sympathetic nervous system.
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PMID:The hypothalamo-sympathetic nervous system modulates peripheral cellular immunity. 869 99

In the psychic stress, ADH releases at the same time with CRF which intensifies the effects of it. Endogenous opioids cause above all the analgesia and paradoxical euphoria of stress. Psychic stress needs through the risk of heart frequency a higher capacity and it aggravates the valvular insufficiency and the valvular stenosis. The patient with rheumatic mitral stenosis could have a genetic psychic location predisposed to a higher vulnerability for psychic stress.
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PMID:[A clinico-etiopathogenic update on mental stress as a cardiovascular risk factor]. 945 94

Tissue damage causes an inflammatory response in which cytokines contribute to a painful state. Local inflammation also leads to an enhanced expression of opioid peptides such as END within immune cells of inflamed tissue. These endogenous substances can be released by "releasing factors" such as CRF and IL-4 via activation of their receptors on the cell surface of inflammatory cells. Local application of CRE or IL-1 into inflamed tissue results in significant analgesia which is most likely mediated by a release of opioid peptides from immune cells within inflamed tissue. This mechanism of pain inhibition also seems to have a physiological role. Upon certain stressful stimuli analgesic effects seem to be mediated by a release of opioid peptides and a subsequent activation of peripheral opioid receptors. Locally expressed CRF but not IL-1 appear to trigger this release. Thus, inflammatory pain can be modulated both by exogenous CRF and IL-1 as well as endogenous CRF. These mechanisms are based on interaction between the immune and nervous systems. Both the initiation of pain and its control can be regarded as the body's response to prevent further injury, to support wound healing and to return to a normal function as quickly as possible.
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PMID:Cytokines and peripheral analgesia. 1261 63

The role of hypothalamic-pituitary-adrenocortical system (HPAS) in analgesic effect induced by central or systemic corticotrophin-releasing hormone (CRH) was studied on anaesthetized male rats. Blockade of the HPAS functional activity by hydrocortisone in pharmacological dose one week before the experiment was used as approach to investigate the contribution of the HPAS hormones in CRF-induced analgesia. Elimination of the hormones rise in the blood plasma by hydrocortisone resulted in decrease of analgesic effect induced by systemic CHR and complete disappearance of analgesic effect induced by central CRH. The results suggest that CRH-induced elevation of pain threshold is provided by two components: 1) depending on the HPAS hormones after central and systemic injection of CHR; 2) not depending on the HPAS hormones after systemic injection of CHR.
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PMID:[The role of hormones of hypothalamic-pituitary-adrenocortical system in analgesic effect of corticotropin-releasing hormone]. 1673 59


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