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)

The effects of the opioid antagonist naloxone on the vasopressin (AVP) and oxytocin (OT) responses to nicotine were studied in male non-smokers (21-30 years old). Either saline (n = 6) or naloxone (4 mg bolus + 6 mg/h, n = 6) was infused i.v. during the study. After 60 min infusion the subjects smoked one high-nicotine content cigarette. Naloxone infusion for 60 min did not alter basal plasma AVP or OT levels. Smoking led to a significant rise in plasma vasopressin in both saline and naloxone-infused subjects (P less than 0.05). There was no significant difference in the plasma AVP response to smoking between the two groups. Saline-infused subjects did not show any change in plasma OT in response to smoking. Naloxone infusion was associated with a significant rise in OT from 1.3 +/- 0.1 pmol/l to 4.3 +/- 2.4 pmol/l 5 min after smoking (P less than 0.05). We conclude that there is endogenous opioid-mediated inhibition of OT which prevents its release when AVP is secreted in response to nicotine in man.
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PMID:Endogenous opioids inhibit oxytocin release during nicotine-stimulated secretion of vasopressin in man. 321 43

1. Rats underwent either: (1) acute or chronic morphine or naloxone administration; (2) simple morphine withdrawal or naloxone-precipitated withdrawal in morphine-dependent animals; or (3) stress from I.P. administration of hypertonic saline. 2. Quantitative in situ hybridization histochemistry was performed using synthetic oligonucleotide probes for corticotrophin-releasing factor (CRF), vasopressin, pro-opiomelanocortin (POMC), dynorphin, enkephalin and oxytocin mRNAs. The paraventricular and supraoptic nuclei were examined in all studies and the arcuate nucleus and pituitary gland in the acute withdrawal study. 3. Neither acute nor chronic morphine administration altered either (a) hypothalamic parvocellular or magnocellular CRF mRNA, or (b) anterior pituitary or pars intermedia POMC mRNA. 4. Naloxone-precipitated morphine withdrawal resulted in a marked increase in parvocellular (but not magnocellular) CRF mRNA within 4 h and levels remained elevated through 24 h. There was no change in arcuate nucleus or pars intermedia POMC mRNA, but in the anterior pituitary there was a delayed increase, significant at 24 h. 5. Simple morphine withdrawal without the use of naloxone did not result in any change in CRF mRNA but there were increases in magnocellular vasopressin and dynorphin mRNA, presumably related to decreased water intake. 6. Intraperitoneal hypertonic saline stress also resulted in a marked accumulation of both parvocellular CRF and vasopressin mRNA without any concomitant change in magnocellular vasopressin mRNA. Increased translation of CRF mRNA was also evidenced by increased immunoreactive CRF detected by immunocytochemistry.
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PMID:Corticotrophin-releasing factor, vasopressin and pro-opiomelanocortin mRNA responses to stress and opiates in the rat. 326 21

Rats were given bilateral injections of colchicine into the area of the nucleus basalis. Colchicine produced dose-dependent alterations in the acquisition of a food-reinforced working-memory task. Colchicine-induced deficits in maze performance were attenuated by cholinergic agents, including physostigmine, RS-86 (2-ethyl-8-methyl-2,8-diazospiro-(4,5)-decan-1,3-dione-hydro bromide) and nicotine. Naloxone and vasopressin did not affect radial-arm maze performance of colchicine-treated rats. Subsequent neurochemical analysis showed that colchicine decreased choline acetyltransferase (ChAT) activity and levels of norepinephrine, dopamine, 3,4-dihydroxyphenylacetic acid, serotonin and 5-hydroxyindoleacetic acid in the neocortex. However, ChAT activity and other neurochemical measures were not altered in the hippocampus or corpus striatum. Histological assessment indicated damage limited to the injection in the area of the nucleus basalis and enlarged cerebrolateral ventricles. These data suggest the possible utility of the colchicine model in the study of cognitive deficits associated with neurodegenerative diseases.
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PMID:Radial-arm maze deficits produced by colchicine administered into the area of the nucleus basalis are ameliorated by cholinergic agents. 334 52

Opioid peptides and cholecystokinin (CCK) have been shown to play a role in regulation of feeding behavior. Another neuropeptide that has recently been suggested to be involved in feeding is vasopressin. We explored possible interactions between opiates, CCK and vasopressin in feeding regulation by studying feeding suppression produced by naloxone and CCK in Brattleboro (DI) rats, which are homozygous for diabetes insipidus and lack the ability to synthesize vasopressin. Ten DI and 15 age-matched Long Evans (LE) rats were food deprived for 14 hours on two different days and then injected with naloxone (2.5 mg/kg) on one day or saline on the other. Thirty minutes later the food was returned and food and water consumption were measured after 1, 3 and 4 hr. Naloxone suppressed the food consumption of both DI and LE rats but the suppression was greater for the DI rats. This result was specific to feeding as water consumption was suppressed in LE more than in DI rats. Two weeks later, the same rats were food deprived for 6 hours on two different days and then injected with CCK-8 (2.5 micrograms/kg) on one day and with saline on the other. Food was returned one minute after the injection and food and water consumption were measured 30 and 60 minutes later. Food intake was reduced equally for both DI and LE rats. Water intake was not reduced. The results suggest that the suppression of feeding by CCK does not require an intact vasopressinergic system. The greater feeding suppression by naloxone in DI rats may suggest that opiates are interacting with vasopressin in producing their effects on food intake.
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PMID:Effects of naloxone and cholecystokinin on food and water intake in vasopressin-deficient rats (Brattleboro strain). 343 22

Immunoreactive oxytocin (OXT) and arginine8-vasopressin (AVP) levels were measured in limbic areas of the mouse brain (hippocampus, amygdala and basal forebrain). Peptides were measured by radioimmunoassay (RIA). Acute morphine treatment caused a naloxone-reversible increase in OXT content in all three brain regions. The AVP contents of the same brain areas, on the other hand, were not affected by acute morphine treatment. In mice rendered tolerant to/dependent on morphine with subcutaneous morphine pellets, the OXT levels in the limbic brain structures were in the control range (basal forebrain and amygdala) or even decreased (hippocampus). In the latter brain structure of the tolerant animals, the AVP content was also decreased. Naloxone-precipitated withdrawal syndrome in the tolerant/dependent animals resulted in abrupt increases in the OXT and AVP levels of the hippocampus and in the OXT content of the basal forebrain structures.
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PMID:Limbic oxytocin and arginine 8-vasopressin in morphine tolerance and dependence. 355 59

The effect of the opiate antagonist naloxone on neurohypophyseal hormone secretion has been investigated in rats given 2% NaCl to drink for 0-9 days. Naloxone elicited a rise in plasma levels of oxytocin (OT), but not arginine-vasopressin (AVP), on days 1-3 only, the greatest response being on day 2. In a further experiment, the OT response to an acute stimulus (1.5 M NaCl, i.p.) was found to be similar in controls and rats drinking 2% NaCl for 7 days, indicating that depletion of readily releasable hormone was not the cause of the loss of sensitivity to naloxone; rather a down-regulation of opiate receptor mechanisms may be responsible. The temporal changes in opiate antagonist-sensitivity in saline-loaded rats may provide a functional paradigm for the investigation of regulatory opiate mechanisms in neural tissue.
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PMID:Temporal changes in the activity of endogenous opioid mechanisms regulating oxytocin secretion in saline-loaded rats. 369 93

Naloxone, an opiate receptor antagonist, was used to determine whether opioid peptides modulate release of oxytocin (OT) or vasopressin (AVP) in the rat after expulsion of the fetus, i.e. parturition. We measured the concentrations of AVP and OT in plasma and in the neurointermediate lobe of the pituitary of pregnant rats given naloxone (5 mg/kg, s.c.) or saline on day 20 of gestation, and on day 21 either before or during the expulsive stage of labor. Non-pregnant rats in diestrus were given naloxone for comparison. On days 20 and 21 of gestation, before the onset of parturition, plasma [AVP] but not [OT] was elevated, compared to the non-pregnant controls. After delivery of the first two pups, plasma [OT] approximately doubled, whereas plasma [AVP] remained unchanged. Blocking the action of endogenous opioid peptides with naloxone caused an elevation of plasma [OT] in pregnant animals on days 20 and 21 of gestation and during parturition. Naloxone, however, did not alter plasma [AVP] in either parturient or preparturient animals. In contrast, [AVP], but not [OT], was increased in plasma of non-pregnant rats given naloxone. The content of OT in the neuro-intermediate lobe was similar in pregnant and non-pregnant rats and was unaffected by delivery of the first two pups. However, AVP content and the ratio of AVP/OT in the pituitary were lower in pregnant animals before and during delivery than in the non-pregnant controls. The content of neither hormone was altered by naloxone. Thus, AVP release apparently increases and pituitary stores of this peptide are decreased by day 20 of gestation, when labor has not yet begun.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of release of neurohypophysial hormones by endogenous opioid peptides in pregnant and parturient rats. 375 22

Endogenous opioid peptides inhibit secretion of oxytocin during dehydration, hemorrhage and parturition and attenuate release of vasopressin by tail electroshock. Diverse agents were used to stimulate the hypothalamo-neurohypophysial system to investigate the hypothesis that if oxytocin (or vasopressin) release were inhibited by opioid peptides regardless of the stimulus, the site of opiate action may be in the final common pathway (i.e. the magnocellular neuron) or on pituicytes in the neural lobe. Using male Sprague-Dawley rats, we therefore investigated the effect of an opiate receptor antagonist, naloxone (5 mg/kg s.c.), on the plasma concentrations of oxytocin and vasopressin elevated by various pharmacologic stimuli, including histamine (10 mg/kg i.p.), nicotine (0.15 or 1.5 mg/kg i.p.), isoproterenol (30 or 120 micrograms/kg i.m.) and increased [NaCl] in cerebrospinal fluid (CSF; 10 microliter artificial CSF containing 1 M NaCl i.v.t.). Control animals received saline (0.85%) or artificial CSF (containing 0.16 M NaCl). Animals were decapitated 60 s (increases[NaCl] in CSF) or 10 min after the stimulus or vehicle. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. The concentrations of oxytocin and vasopressin in plasma were elevated (p less than 0.05) by histamine, isoproterenol (30 and 120 micrograms/kg), increases[NaCl] in CSF, and nicotine at the higher (1.5 mg/kg) but not lower (0.15 mg/kg) dose. Naloxone increased further (p less than 0.05) the concentration of oxytocin in plasma after histamine, nicotine (0.15 and 1.5 mg/kg), isoproterenol (30 and 120 micrograms/kg) and increases[NaCl] in CSF. Naloxone also increased (p less than 0.05) oxytocin concentration in controls receiving CSF or saline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Naloxone effects on plasma vasopressin and oxytocin concentrations elevated by histamine, nicotine, isoproterenol and an acute increase in [NaCl] in cerebrospinal fluid. 379 91

Intracerebroventricular injections of morphine (5-20 micrograms) produced a dose dependent antidiuresis in the conscious hydrated rat. Naloxone pretreatment completely abolished this antidiuretic effect, but pretreatment with a specific antidiuretic vasopressin antagonist did not change the morphine antidiuresis. The vasopressin concentration in the first voided urine after antidiuresis from morphine treated rats was found to be in the same range as the vasopressin concentration in urine from saline treated rats. Injections of 20 micrograms morphine intracerebroventricularly in conscious hydrated rats gave a short decrease in heart rate but not in mean arterial blood pressure. This indicates, that either liberation of vasopressin nor a fall in systemic blood pressure contribute to the morphine antidiuresis.
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PMID:Morphine antidiuresis in conscious rats: contribution of vasopressin and blood pressure. 397 2

The hypothalamo-neurohypophysial system is altered in the spontaneously hypertensive rat (SHR). We hypothesized that an aberrant regulation of vasopressin (VP) and oxytocin (OT) release by endogenous opioid peptides alters this neuroendocrine system in the SHR. Concentrations of the neurohypophysial hormones in plasma and the pituitary were measured in 17-week-old SHRs and two strains of normotensive controls. Wistar Kyoto (WKY) and Sprague-Dawley rats. Animals were decapitated 20 min after s.c. injection of saline (1 ml/kg) or naloxone hydrochloride (1 or 10 mg/kg). In addition, neurohypophysial hormones excreted during the day (08.00-17.30 h) and night (17.30-08.00 h) were determined in urine from 16-week-old animals kept in metabolic cages for 5 days. VP at extrahypothalamic sites was also measured as [VP] in acid extracts of the subfornical organ area, hippocampal commissure-fornix and choroid plexus. Hormones were quantified by radioimmunoassay. The pituitary content, plasma concentration, and urinary excretion of OT were reduced (P less than 0.05) in SHRs, whereas VP content was increased (P less than 0.05) in the pituitary and plasma, but unchanged in urine, of hypertensive animals. In extrahypothalamic tissues, [VP] in the hippocampal commissure-fornix was increased in the SHR. Naloxone elevated (P less than 0.05) the plasma concentration of OT in WKY animals and VP in SHRs. Neither [VP] nor [OT] in plasma was changed by naloxone in Sprague-Dawley rats. Pituitary stores of the neurohypophysial hormones were not altered by naloxone in either hypertensive or normotensive rats. In conclusion, endogenous opioid peptides tonically inhibit OT release in WKY rats, whereas VP release is decreased by opioid peptides in SHRs, 16-17 weeks of age. The neuromodulatory role of opioid peptides in the release of neurohypophysial hormones appears to be altered in the SHR such that VP release is suppressed and OT release is augmented.
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PMID:Differential effects of naloxone on the release of neurohypophysial hormones in normotensive and spontaneously hypertensive rats. 397 14


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