Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were carried out to investigate whether vasopressin is involved in stress-induced analgesia. Intraperitoneal injection of hypertonic saline caused a significant and dose-related increase in the latency to the tail-flick response of the rat to noxious heat and was used as a stimulus for stress-induced analgesia. Neither the pituitary nor opioid peptides appeared to be involved, since the response occurred in hypophysectomized rats and was not reduced by the opiate antagonist naloxone. Furthermore hypertonic-saline analgesia was clearly potentiated in hypophysectomized rats in comparison to sham-operated controls. Hypertonic-saline analgesia was also observed in vasopressin-deficient (homozygous Brattleboro) rats similar in both magnitude and duration to that in normal rats of the same strain (Long Evans). It was concluded that vasopressin was not involved in stress-induced analgesia evoked by hypertonic saline.
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PMID:Stress-induced analgesia evoked by intraperitoneal injection of hypertonic saline: evidence for its occurrence in vasopressin deficient rats. 403 7

Desglycinamide(9)-lysine vasopressin facilitates development of resistance to the analgesic action of morphine in mice if morphine is administered before the peptide. Desglycinamide(9)-lysine vasopressin is not a morphine antagonist, and does not appear to cause either hyperalgesia or alteration of the response to the technique used for evaluating analgesia.
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PMID:Facilitation of development of resistance to morphine analgesia by desglycinamide9-lysine vasopressin. 452 67

Several laboratories have reported that dynorphin and vasopressin may be present in the same neurons and released together in a fixed ratio. In this study, we report that vasopressin and dynorphin can regulate morphine-induced analgesia in the mouse tail-flick test. Its action is opposite that observed for dynorphin because, when administered simultaneously with morphine, vasopressin in a dose-related manner potentiated morphine-induced analgesia while dynorphin antagonized it. When vasopressin and dynorphin is administered together with morphine, morphine ED50 returned to control level.
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PMID:Possible physiological control of morphine analgesia in mice. 612 49

Opioid analgesics influence the function of a number of neurotransmitter systems including classical neurotransmitters, neuropeptides and endogenous opioids. The role of these interactions in analgesia, tolerance and dependence is reviewed. Opioids inhibit the release of substance P from high threshold primary afferents, depress the activity of dorsal horn neurons and increase activity in serotonergic and noradrenergic neurons projecting from brainstem to spinal regions. Chronic administration of opioids modifies the dynamics of classical transmitters and those of endogenous opioid peptides in the brain, spinal cord and the pituitary gland. However, the effects observed are very variable. Several neuropeptides (vasopressin, MIF, alpha-MSH, CCK and dynorphin) have been reported to modify acute and chronic effects of opioids. Tolerance and dependence seen after opiate administration may involve changes in the function of these peptides.
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PMID:Opioid-neurotransmitter interactions: significance in analgesia, tolerance and dependence. 615 40

A syndrome of disordered hypothalamic function with abnormal control of temperature, appetite, and thirst, hyperprolactinaemia, and inappropriate vasopressin release is described in a 13-year-old boy who, in addition, had insensitivity to pain and a more general disorder affecting mood, sleep, and control of respiration. A disturbance of the opioid peptide system is postulated. Naloxone reversed central analgesia, altered urine fluid and electrolyte excretion, modified the hormonal response to gonadotrophin-releasing and thyrotrophin-releasing hormones, and improved the auditory and visual reaction times. Specific opioid antagonists may have a therapeutic role.
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PMID:Effect of naloxone in a previously undescribed hypothalamic syndrome. A disorder of the endogenous opioid peptide system? 615 79

Substance P(SP), the heptapeptide SP and the stable analogue (p-Glu5-MePhe8-MeGly9) SP (DiMe-C7) induce a Ca2+-dependent release of Met5-enkephalin (MET) from slices of periaqueductal gray matter (PAG) and striatum of rats. The MET release from striatal slices is greater than that from PAG slices because of the higher MET content of striatum. Intraventricular injection of SP and of the two related peptides induce analgesia in the rat, and their analgesic potency is in line with their capacity to release MET. Other neuropeptides which possess antinociceptive activity such as bombesin, neurotensin, vasopressin and somatostatin fail to release MET from PAG slices.
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PMID:Substance P-induced release of Met5-enkephalin from striatal and periaqueductal gray slices. 619 90

Opiate receptors in the central nervous system may be classified according to pharmacological, behavioural, or binding studies. Classical mu-receptors probably have beta-endorphin as an endogenous ligand, and seem to be involved in the modulation of pain perception, low-frequency acupuncture analgesia, and the stimulation of prolactin, growth hormone and thyroid-stimulating hormone release. Met-enkephalin is likely to be an endogenous ligand for the delta-receptors, which predominate in the basal ganglia and limbic systems; such receptors may tonically inhibit the release of corticotrophin-releasing factor. It has been suggested that the newly-described kappa-receptors may inhibit the release of vasopressin and gonadotrophin-releasing factor; dynorphin may be their endogenous ligand. Endogenous opiates controlling cardiovascular and respiratory reflexes are likely to activate mu-receptors, while high-frequency acupuncture may alleviate the symptoms of opiate withdrawal by allowing an increase in Met-enkephalin to activate delta-receptors. In the periphery, beta-endorphin is concentrated in the corticotrophs of the anterior pituitary, and is cosecreted with ACTH and related peptides. Circulating Met-enkephalin originates in the gut, sympathetic nervous system and adrenal medulla. Met-enkephalin may also be extracted from carcinoid tumours and phaeochromocytomas. Elevations in circulating Met-enkephalin may occur in certain disease states with cardiovascular and psychiatric manifestations. However, manipulation of endogenous or exogenous opiates has as yet no certain place in any clinical situation.
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PMID:Opiate receptors: enkephalins and endorphins. 630 48

This study tested the possibility that beta-endorphin is involved in the regulation of vasopressin release during stress induced by inescapable electric foot shock. To this end, a specific anti-beta-endorphin antiserum or a control serum lacking the specific anti-beta-endorphin antibodies was administered to male rats. Plasma vasopressin concentrations, measured by radioimmunoassay, were not affected by brief foot shock stress in control rats, but were raised significantly by the stress in animals which had received an intracerebroventricular (i.c.v.) injection of the anti-beta-endorphin antiserum. In contrast, when the same volume of the anti-beta-endorphin antiserum was injected into a tail vein, foot shock stress produced only a slight effect on vasopressin release. I.c.v. injection of the antiserum changed neither basal nociceptive threshold nor stress-induced analgesia as revealed by the tail-flick latency. Vasopressin release induced by an osmotic stimulus was not influenced by the anti-beta-endorphin antiserum given i.c.v. The opiate antagonist naloxone or the glucocorticoid dexamethasone raised plasma vasopressin concentration in stressed rats which had received the control serum (i.c.v.); however, after i.c.v. injection of the anti-beta-endorphin antiserum neither naloxone nor dexamethasone elevated the plasma vasopressin concentration beyond the level reached by the anti-beta-endorphin antiserum (i.c.v.) alone. These results suggest that beta-endorphin inhibits the release of vasopressin during foot shock-induced stress in the rat.
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PMID:beta-Endorphin controls vasopressin release during foot shock-induced stress in the rat. 631 22

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.
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PMID:Vasopressin analgesia: specificity of action and non-opioid effects. 649 25

A modification of neuroleptanalgesia by substituting fentanyl with buprenorphine is presented. Both anaesthesia techniques could be applied alternatively. We did not recognize any significant difference between the two groups concerning haemodynamics, the secretion of the so called stress hormones (antidiuretic hormone, cortisol) as well as the postoperative respiratory depression. The long lasting analgesia, which could be achieved by buprenorphine, can be advantageous in certain surgical interventions. The lack of a potent antagonist for buprenorphine in addition to its longer half-life for--not being of advantage in any anaesthesia--is discussed.
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PMID:[Modified neuroleptanalgesia with buprenorphine]. 681 64


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