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)

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

The opioid peptide endorphins, enkephalins, and dynorphins--found in brain, pituitary, and gut--are neurohormones involved in the regulation of a number of seemingly diverse biologic activities, including respiration, mood, pain perception, blood pressure, body temperature, and certain visceral responses. When viewed in integrated fashion, however, the spectrum of activities induced by the administration of both the exogenous opiates (e.g. morphine) and the endogenous opioids resembles a natural physiologic state: the sleep state. We propose that the opioid peptides in conjunction with the peptide neurohormone vasopressin are involved in the induction and maintenance of the sleep state. We also propose that the function of sleep is to protect an animal during periods when it is at a selective disadvantage, and we provide evidence to support and integrate both concepts.
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PMID:Possible role of the opioid peptides in sleep. 647 55

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

Both vasopressin and PGF2 alpha are effective uterine stimulants in the non-pregnant human uterus, especially around the onset of menstruation. In order to clarify the relationship of these hormones to menstrual pain, plasma concentrations of vasopressin and two prostaglandin metabolites (15-keto-13,14-dihydro-PGF2 alpha and 11-ketotetranor PGF metabolites) were measured in serial blood samples taken premenstrually and during menstruation. Five women with premenstrual pain gave 7-9 blood samples at intervals of 30 minutes on the day preceding the onset of menstruation. From 5 women with severe primary dysmenorrhea a corresponding series of blood samples were taken during the first day of menstruation. Two groups of 5 women with no symptoms served as controls, either premenstrually or during menstruation. In the women with premenstrual pain the vasopressin concentrations were significantly higher than in the corresponding control group. Even higher and markedly fluctuating vasopressin levels were found in the women with dysmenorrhea who, in general, had more intense pain than the women with premenstrual symptoms. In the group with dysmenorrhea there was also a significant rise in plasma concentration of the PG metabolites. No such increase was seen in the group with premenstrual pain. It is concluded that the pathophysiology of premenstrual pain could imply increased vasopressin secretion. The more severe pain in primary dysmenorrhea seems to be the result of a combined effect of vasopressin and PGF2 alpha.
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PMID:Vasopressin and prostaglandins in premenstrual pain and primary dysmenorrhea. 654 95

The involvement of prostaglandins (PG) in the vasopressin (VP) action on the human uterus was investigated in healthy women during three menstruations. Intrauterine pressure was recorded and total pressure area measured. Repeated plasma samples were taken for estimations of arginine(A)- and lysine(L)-VP, 15-keto-13,14-dihydro-PGF2 alpha and 11-ketotetranor PGF metabolites. During the first menstruation LVP was infused in a dose of 0.08 micrograms/min. During the second menstruation the infusion of LVP was repeated with the same dose, but 70 min before infusion the women received an oral dose of 500 mg of naproxen. During the third menstruation PGF2 alpha was administered intravenously in a dose of 25 micrograms/min. LVP infusion per se caused a significant increase in uterine activity and plasma levels of LVP and PG metabolites. When the women were pretreated with naproxen practically the same uterine activity was induced and closely similar plasma levels of LVP were obtained, but the levels of PG metabolites decreased significantly in comparison with the first series of experiments. Infusion of PGF2 alpha caused an increase in uterine activity but no change in the plasma levels of AVP. The results indicate that uterine stimulation with VP is possible without an obligatory last step of PG synthesis and release. The results also support the concept that an elevated VP level in primary dysmenorrhoea may be of aetiological importance and is not just released as a 'stress'-hormone because of the dysmenorrhoeic pain.
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PMID:Involvement of prostaglandins in vasopressin stimulation of the human uterus. 657 82

Fifty consecutive patients with metastatic carcinoma who underwent cryohypophysectomy were studied. Of these, 26 had breast cancer, 19 had prostatic cancer, one had malignant melanoma, one had cancer of the kidney, and three had metastatic adenocarcinoma from an unknown primary tumour. After cryohypophysectomy, excellent pain relief was obtained in 48% of patients, good or acceptable pain relief was obtained in 40%, and poor or no relief in 12%. Two patients died: one of aspiration pneumonia and one of an unknown cerebral cause. Sixteen patients developed diabetes insipidus, of whom three required therapy with vasopressin; eight patients developed a cerebrospinal fluid leak, two of whom required surgical repair; and four patients developed meningitis, which resolved in three after antibiotic therapy. Results are compared with those from other published reports. Pain relief from cryohypophysectomy is surmised to be due to the production of endorphins, but no proof of this is available.
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PMID:Cryohypophysectomy for the relief of pain in malignant disease. 669 92

We treated 25 patients with ureteral colic and urographically verified stones with 50 mg. indomethacin intravenously. Pain was relieved completely in 17 patients, while in 8 incomplete or no pain relief was achieved after the infusion of indomethacin. Patients completely relieved of pain had significantly higher levels of antidiuretic hormone in plasma before the infusion of indomethacin (18.2 plus or minus 3.4 pg./ml.) than patients with incomplete or no pain relief (7.2 plus or minus 1.3 pg./ml.) (p less than 0.01). These findings indicate that the volume status and/or the level of antidiuretic hormone may be of critical importance for pain relief after infusion of indomethacin in patients with ureteral colic.
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PMID:Antidiuretic hormone levels and the effect of indomethacin on ureteral colic. 685 62

Systemically administered lysine-8-vasopressin (LVP; 16-128 micrograms/kg) was found to induce a potent and dose-dependent antinociceptive effect, as measured by the tail-flick test in the rat. This effect could be seen in the absence of any significant change in general activity, indicating that it was not due to sedation or general motor debilitation. The antinociceptive effect of LVP does not appear to be mediated by endogenous opiates or other pituitary hormones, as evidenced by: 1) the lack of antagonism by the opiate receptor blocker naloxone, 2) the lack of cross-tolerance with morphine, and 3) its persistence after hypophysectomy. Des-glycinamide-LVP, a vasopressin analog with no appreciable pressor or antidiuretic action, showed no antinociceptive activity (128 micrograms/kg), and des-amino-arginine-vasopressin, a vasopressin analog with minimal pressor activity but greatly enhanced antidiuretic activity, was also relatively ineffective (128 micrograms/kg). These results suggest that the antinociceptive activity of vasopressin may be related to receptor types similar to those mediating its pressor effects. Nevertheless, the antinociceptive action of vasopressin does not appear to be secondary to its pressor activity, since phenylephrine failed to induce an antinociceptive effect at a dosage that mimicked the pressor response to vasopressin. These results are in concert with a growing body of evidence suggesting that vasopressin may be one of several nonopiate peptides that play a role in the modulation of pain sensitivity.
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PMID:Vasopressin-induced antinociception: an investigation into its physiological and hormonal basis. 686 6

The role of techniques used for management of intra- and postoperative pain on plasma levels of antidiuretic hormone (ADH) was evaluated in 107 patients undergoing abdominal or thoracic surgery. Fifty-one patients had neurolept-anesthesia (NLA) intraoperatively followed by intramuscular piritramide, a long-lasting synthetic narcotic, for relief of postoperative pain. Fifty-six patients had a combination of epidural bupivacaine and NLA intraoperatively followed by epidural fentanyl for relief of postoperative pain. All patients had daily measurements of serum levels of potassium and sodium, plasma levels of ADH, and plasma osmolality for the first 5 postoperative days. In 67 patients arterial blood-gas tensions also were measured at similar times. There were no significant changes in serum electrolyte levels, plasma osmolality, or blood-gas tensions intra- or postoperatively. Plasma ADH levels increased postoperatively in all patients, but in patients given NLA followed by postoperative intramuscular narcotics, plasma levels of ADH were more than twice as great as in patients given epidural anesthesia followed by epidural fentanyl.
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PMID:Influence of epidural fentanyl on stress-induced elevation of plasma vasopressin (ADH) after surgery. 686 58

A synthetic analogue, deamino-ethyl-oxytocin, which competitively inhibits vasopressin action on uterine activity both in vitro and in animal experiments was developed. The uterine effect of this analogue was studied during the recording of intrauterine pressure in 16 gynecologically healthy women. Increased uterine activity and dysmenorrhea-like pain was induced by infusing lysine vasopressin in a dose of 0.08 microgram/min. Deamino-ethyl-oxytocin inhibited vasopressin action, the threshold dose being approximately 200 micrograms given as a single intravenous injection for about 20 minutes. When given intranasally the drug was also shown to be effective in inhibiting vasopressin-induced uterine activity and symptoms. These results suggest that deamino-ethyl-oxytocin could be of therapeutic value in primary dysmenorrhea, a condition associated with increased vasopressin secretion.
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PMID:Inhibition of vasopressin effects on the uterus by a synthetic analogue. 687 87


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