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 mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin(PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 microgram/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 microgram/kg). Ten human subjects experienced nausea after 16 microgram/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 microgram/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 microgram/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine doses of 200 microgram/kg induced only slight increases in PAVP when compared to the response to 16 microgram/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.
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PMID:Influence of the emetic reflex on vasopressin release in man. 54 11

1. The rat hypothalamus (containing the supra-optic nuclei, paraventricular nuclei, median eminence and proximal pituitary stalk) has been incubated in vitro and shown to be capable of releasing the neurohypophysial hormones, oxytocin and arginine vasopressin, at a steady basal rate about one twentieth that of the rat neural lobe superfused in vitro. 2. The hypothalamus and neural lobe in vitro released both hormones in a similar arginine vasopressin/oxytocin ratio of about 1-2:1. However, when release was expressed relative to tissue hormone content, the hypothalamus was shown to release about three times as much arginine vasopressin and six times as much oxytocin as the neural lobe. 3. Dopamine in a concentration range of 10(-3)-10(-9)M caused graded increases in hormone release from the hypothalamus in vitro to a maximum fivefold increase over preceding basal levels. The demonstration that apomorphine also stimulated hormone release whereas noradrenaline was relatively ineffective suggested that a specific dopamine receptor was involved. A separate cholinergic component in the release process was indicated by the finding that acetylcholine stimulated release to a maximum fivefold increase in concentrations of 10(-3)-10(-9)M. 4. The fact that the isolated hypothalamus can be stimulated by dopamine and acetylcholine to release increased amount of oxytocin and arginine vasopressin raises the question of the origin and fate of the hormones released in this way. The possibility that they could be released into the hypophysial portal circulation from median eminence to affect the anterior lobe of the pituitary is discussed. 5. In similar doses, both dopamine and noradrenaline injected into the lateral cerebral ventricles of the brain of the anaesthetized, hydrated, lactating rat caused the release of arginine vasopressin and oxytocin. Apomorphine release both hormones but at a higher dose level and to less effect than the catecholamines. 6. The hormone release induced in vivo by dopamine could be prevented by the prior administration of haloperidol or phentolamine and these antagonists were equally effective in blocking the hormone release due to noradrenaline. The involvement of a specific dopamine receptor was more clearly implicated by the use of pimozide which completely inhibited the hormone release due to dopamine and apomorphine but not that due to noradrenaline. 7. It is suggested that the release of neurohypophysial hormones can be stimulated via a dopaminergic nervous pathway in addition to a cholinergic one. The possibility that the osmoreceptor mechanism for the release of antidiuretic hormone from the neural lobe of the pituitary may involve such a dopaminergic pathway is discussed.
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PMID:The effect of dopamine on neurohypophysial hormone release in vivo and from the rat neural lobe and hypothalamus in vitro. 98 83

Apomorphine challenge tests (0.5 mg SC) were performed in 14 normal male volunteers and in 9 male schizophrenic inpatients, drug-free for at least 2 wk. In the normal volunteers, apomorphine induced an increase of serum growth hormone (GH) (maximum at 40 min), of vasopressin-neurophysin (hNpI) (maximum at 20 min), and oxytocin-neurophysin (hNpII) (maximum at 20 min). The release of neurophysins was independent of digestive side effects. In the schizophrenics, the GH level and release pattern were similar to those in the controls. The basal level of hNpI was reduced (t0: 0.42 +/- 0.1 ng/ml in the schizophrenics and 0.66 +/- 0.05 ng/ml in the controls, p < 0.02). In contrast, the basal level of hNpII was increased (3.34 +/- 0.04 ng/ml in the schizophrenics to 0.92 +/- 0.21 ng/ml in the controls, p = 0.001). The response to apomorphine was blunted, with no significant release of hNpI or of hNpII. Although the hNpII data are consistent with an increased dopaminergic tone, the psychopathological meaning of the increased basal oxytocinergic and decreased vasopressinergic functions remains to be defined.
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PMID:Apomorphine stimulation of vasopressin- and oxytocin-neurophysins. Evidence for increased oxytocinergic and decreased vasopressinergic function in schizophrenics. 128 81

Bromocriptine (5-100 microgram; 6.7 X 10(-9) - 1.3 X 10(-7) mol.), SK&F 38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine, 0.5-5 mg; 1.7 X 10(-6)-1.7 X 10(-5) mol.) and apomorphine (20-200 microgram; 6.4 X 19(-8)-6.4 X 10(-7) mol.) administered into rat kidneys perfused with physiological solution containing vasopressin and pretreated with an alpha-adrenoreceptor antagonist produced vasodilator responses similar to dopamine (50-100 microgram; 2.6 X 10(-8)-5.3 X 10(-7) mol.). THe responses to bromocriptine, SK&F 38393 and apomorphine were found to be significantly reduced by the dopamine receptor antagonist ergometrine (50 microgram; 1.1 X 10(-7) mol.). Metoclopramide (250 microgram; 7.4 X 10(-7) mol.) was found to be an effective antagonist of dopamine, bromocriptine, SK&F 38393 and apomorphine. Apomorphine (20, 50 microgram; 6.4 X 10(-8), 1.6 X 10(-7) mo.) was found to act as a partial agonist on dopamine receptors in this preparation.
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PMID:A comparison of the responses to some dopamine-receptor agonists and antagonists in the isolated perfused rat kidney. 697 30

1. A transient increase in plasma vasopressin concentrations represents a physiological correlate of nausea in animals that vomit. 2. The CCKA receptor antagonist devazepide has previously been shown to inhibit vasopressin release induced in pigs by intravenous (i.v.) CCK. 3. This study investigated whether devazepide (70 micrograms/kg i.v.) would affect vasopressin secretion induced in pigs (n = 6) by the emetic drug apomorphine (25 micrograms/kg i.v.). 4. Apomorphine stimulated vasopressin release in the 30 min period following injection; this effect was prevented by prior administration of devazepide. 5. The results suggest that CCKA receptor antagonists may have the ability to prevent nausea and/or emesis.
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PMID:The CCKA receptor antagonist devazepide inhibits the effect of apomorphine on vasopressin release in pigs. 789 43

Nauseogenic agents, such as apomorphine, were previously reported to promote peripheral release of oxytocin (OT), but not vasopressin (AVP) in rats, and AVP, but not OT in humans (7-13). In the present study, we compared the peripheral secretory responses of OT and AVP in adult male and female rhesus and male cynomolgus monkeys administered graded doses of apomorphine and the respective dopamine D1 and D2 receptor agonists, CY 208-243 and LY 163502. Apomorphine (50-400 micrograms/kg) and LY 163502 (10-100 micrograms/kg) elicited dose-dependent stimulation of OT and AVP, whereas CY 208-243 did not significantly increase secretion of either hormone. The magnitude of the OT and AVP secretory response varied among the animals. Peripheral OT and AVP responses were robust, but the magnitude of the secretory responses was greater for AVP than OT. None of the animals displayed emetic behavior during the studies. These studies indicate that dopaminergic stimulation, particularly of D2 receptors, can regulate both AVP and OT secretion in monkeys.
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PMID:Oxytocin and vasopressin secretion in monkeys administered apomorphine and a D2 receptor agonist. 809 18

The ferrets' responsiveness to several known and putative emetic agents was evaluated using a variety of agents that were injected subcutaneously and/or intravenously. Apomorphine was consistently emetic at relatively high doses (100 micrograms/kg) when injected subcutaneously in large male ferrets (> or = 1.4 kg). The responsiveness to apomorphine was anomalous in that subcutaneous injections produced a more consistent response than intravenous ones. In addition, ferrets rapidly become tolerant or tachyphylactic to subcutaneously administered apomorphine. Area postrema ablation, but not abdominal vagotomy, rendered ferrets refractory to the emetic effects of apomorphine. This species, relative to dog and humans, proved to be insensitive to a variety of pharmacologic agents including angiotensin II, gastrin, histamine, Leu-enkephalin, neurotensin, serotonin, and vasopressin. Cisplatin elicited forceful retching and emesis. Emetic responses were obtained with substance P and Met-enkephalin in individual animals but were inconsistent. Sensitivity to DAGO [D-Ala2,MePhe4,Gly-ol5 enkephalin] was variable. Results of this study indicate that the ferret is not an optimal model for all forms of emesis.
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PMID:Behavioral studies of emetic sensitivity in the ferret. 849 72

A number of studies have reported abnormalities of neurohypophyseal secretions in major depressive disorder. The purpose of the present study was to test the influence of apomorphine and clonidine injections on plasma vasopressin (AVP)-neurophysins and oxytocin(OT)-neurophysins levels, as direct index of posterior pituitary activation in major depression. Apomorphine and clonidine tests were carried out in 25 medication-free depressive patients and 25 age and gender-matched healthy controls. Blood for neurophysins analysis was drawn by venipuncture at t0, t + 20, t + 40, t + 60 and t + 120. Baseline AVP-neurophysins concentrations were significantly lower in depressives (0.12 +/- 0.14 ng/ml) than in healthy subjects (0.24 +/- 2.15 ng/ml) (p < 0.04). The response to apomorphine test revealed a significant reduced response at 20 (p = 0.01), 40 (p = 0.007) and 60 (p = 0.02) and 120 (p = 0.02)min. Following clonidine test, post hoc tests also revealed a significant decrease at 0 (p = 0.04), 20 (p = 0.01), 40 (p = 0.007) and 60 (p = 0.02) and 120 (p = 0.006)min. Concerning OT-neurophysins, no significant differences were found between depressed and controls in response to clonidine or apomorphine injections. Following clonidine and apomorphine, major depressives exhibited a significantly lower peak GH response than controls. The study supports partially the hypothesis of a reduced vasopressinergic activity in depression. Moreover, we did not find any influence of acute apomorphine or clonidine injections on vasopressin-neurophysin or oxytocin-neurophysin in depressive patients.
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PMID:AVP- and OT-neurophysins response to apomorphine and clonidine in major depression. 1596 47