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)

Mice were rendered physically dependent on ethanol by inhalation of ethanol vapour and treatment with pyrazole for 3 days. On Day 4, withdrawal convulsions were measured and on Day 5 or later, residual tolerance to the hypothermic effect of an i.p. challenge dose of 3 g/kg ethanol was assessed. Mice continuously infused with the vasopressin fragment des-Gly9-[Arg8]-vasopressin dicitrate (DGAVP) throughout the periods of dependence induction and withdrawal testing exhibited exacerbated withdrawal convulsions. DGAVP also tended to exacerbate withdrawal when injected s.c. repeatedly (10 micrograms/injection/mouse) during testing for withdrawal. The data indicate that these effects were not likely to have been due to subconvulsive activity of DGAVP by itself or to changes in blood levels of ethanol. Continuous infusion of DGAVP enhanced residual tolerance on Day 5 but did not maintain tolerance when the time interval between withdrawal and testing for tolerance was increased. Restricting treatment with DGAVP to the period of induction of dependence (Days 1-3) also enhanced tolerance on Day 5. The data indicate that the vasopressin fragment modulates the development and/or the decay of tolerance to ethanol. In addition it exacerbates withdrawal convulsions, an effect that may be due to modulation of physical dependence.
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PMID:Tolerance to ethanol and severity of withdrawal in mice are enhanced by a vasopressin fragment. 719 31

The influence of GABA and of drugs, known to alter GABA-metabolism, on the hypovolaemia-provoked vasopressin release was investigated in rats. Blood volume was decreased without altering plasma osmolality or arterial blood pressure by i.p. injection of polyethylene glycol and the resulting plasma vasopressin concentration was measured using a radioimmunoassay. I.c.v. injections of GABA (0.4-2 mg) markedly suppressed the hypovolaemia-induced vasopressin release. The central inhibitory effect of GABA could not be related to appropriate changes in peripheral parameters believed to regulate vasopressin release (arterial blood pressure, renin-angiotensin system). Aminooxyacetic acid (9-81 mg kg-1, i.m.) and gamma-vinyl-GABA (1.5 g kg-1, i.p.), two potent inhibitors of GABA aminotransferase and known to increase brain GABA content, reduced vasopressin release to a comparable degree as did GABA (i.c.v.). On the other hand, 3-mercaptopropionic acid (10-90 mg kg-1, i.p.), an inhibitor of the GABA synthetizing enzyme glutamic acid decarboxylase, promoted the release of vasopressin when the rats were killed prior to the onset of convulsions. These results, on the whole, intimate the existence of a GABA-mediated inhibition in the central control of vasopressin release.
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PMID:Evidence for the involvement of a GABA-mediated inhibition in the hypovolaemia-induced vasopressin release. 719 56

The authors report on 21 cases of self-induced water intoxication and cite 25 others in the literature. Three of their patients demonstrated at least temporary inappropriate antidiuretic hormone secretion, 3 were receiving a diuretic, and the other 15 appeared to have "pure" water intoxication. Fifteen patients were receiving a psychotropic medication. Self-induced water intoxication appears to be more common in schizophrenic patients than is generally realized and should be suspected in any schizophrenic patient who develops convulsions or coma. Hyperdopaminergic CNS activity may be involved, and the authors suggest a possible mechanism similar to that for tardive dyskinesia.
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PMID:Self-induced water intoxication in schizophrenic patients. 742 54

There is an increasing interest on one of the smallest human chromosomes as it is shown by the First International Symposium on the Human Chromosome 20 and by the genetic map prepared by EUROGEN. The conserved part of the long arm of human chromosome 20 is synthenic with the distal part of the mouse chromosome 2 allowing for some analogies between them. Human chromosome 20 contains several important genes for the human pathology. Mutations of one of them, the vasopressin-neurophysin II gene, are responsible for hereditary neurohypophyseal diabetes insipidus. Severe combined immunodeficiency due to adenosin deaminase deficiency is the first human disorder successfully treated by somatic gene therapy. Spongiform encephalopathies are related to mutation and/or polymorphisms of the PRNP amyloid gene. One form of benign familiar neonatal convulsions is mapped to a specific locus on chromosome 20. In some families, maturity onset diabetes of the young (MODY) is caused by alterations of a hypothetical gene closely linked to the ADA locus. Allegile syndrome is often associated with deletions and microdeletions of the short arm of the chromosome. Finally, deletions of the long arm of the chromosome is a frequent finding in several hematologic malignities, specifically in myeloproliferative disorders and myelodysplastic syndromes.
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PMID:[The human genome--chromosome 20]. 748 83

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

A 59-year-old woman had chronic hyponatremia from inappropriate secretion of antidiuretic hormone (SIADH) and malnutrition after recurrent cholecystitis for 2 months. She developed dysarthria, dysphagia, bilateral ptosis, clonic convulsions and delayed onset Parkinsonian features. Magnetic resonance imaging showed increased signal density in the central pons on T2-weighted images. She was also later diagnosed as having systemic lupus erythematosus (SLE). This case is reported because central pontine myelinolysis (CPM) developed in chronic hyponatremia without correction, and manifested with atypical, delayed-onset Parkinsonian features. The patient recovered well from her neurological illness, unlike the poor outcome in previously reported cases of CPM. In addition, the coincidence of CPM and SLE has not, to knowledge, been reported before.
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PMID:Central pontine myelinolysis in chronic hyponatremic patient: a case report. 771 99

The time course and extent of changes in plasma prolactin, noradrenaline, vasopressin and oxytocin levels is reported following serial observations of a prolonged epileptic seizure arising in the temporal lobe, recorded by video-EEG-telemetry, in which the epileptic activity evolved from a simple partial to complex partial to secondarily generalised attack. The prolactin levels were markedly elevated during the phase of the simple partial seizure, at a time when consciousness was preserved, when motor activity was minimal and when EEG activity was highly localised. The hormonal levels continued to rise during the subsequent seizure evolution, suggesting that the duration (or intensity) of the seizure is an important, perhaps the most important, factor determining the degree of prolactin release during limbic seizures. Indeed, the prolactin elevation in this case (26 times the baseline level) is higher than any previously recorded, reflecting the unusual duration and intensity of this seizure. We did not observe the phenomenon of "exhaustion" of prolactin release and levels peaked after 49 min, and were high for over 2 h after the onset of the seizure, and after the convulsion had ceased. The concentrations of vasopressin, oxytocin and noradrenaline remained low during the aura, but rapidly increased during the phase of generalisation. The oxytocin and noradrenaline levels peaked during the phase of generalised convulsion, but the vasopressin levels peaked well into the post ictal phase, and remained high for several hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentrations of prolactin, noradrenaline, vasopressin and oxytocin during and after a prolonged epileptic seizure. 780 41

A young quadriplegic patient developed convulsions and brain damage due to severe hyponatraemia. Potential causes of severe hyponatraemia in quadriplegics include excessive water intake (because of the low threshold for vasopressin release) and asymptomatic renal tract infection causing sodium loss. Mild hyponatraemia, occurring in up to 10% of quadriplegics, is due to a reset osmostat.
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PMID:Severe hyponatraemia in a quadriplegic. 817 89

Bacterial meningitis has special clinical features in the newborn infant. Major complications and sequelae result from the infectious involvement of the CNS in the majority of these children. We studied 109 newborn infants with bacterial meningitis accompanied from January 1977 to April 1987. The mortality rate was 34.8%. Perinatal risk factors were not found. The majority (80.5%) were term newborn infants. The main signs at admission were convulsion (53.2%), bulging fontanel (37.6%) and apnea (20.2%), and the main symptoms were neurosensorial depression (64.2%), nursing refuse (64.2%), fever (50.5%) and irritability (35.8%). Complications during hospitalization were ventriculitis (34.9%), inappropriate antidiuretic hormone secretion syndrome (27.5%), subdural collection (8.3%), brain abscess (4.6%) and brain infarction (2.8%). Inappropriate antidiuretic hormone secretion syndrome and ventriculitis were closely associated with high mortality. Seventy one children survived: 44 (62%) had gross abnormalities at the neurologic examination, and 29 (40.8%) developed hydrocephalus. Neurological follow-up of these children is important. Prognostic can change along the course of long time follow-up.
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PMID:[Bacterial meningitis in the neonatal period. Clinical evaluation and complications in 109 cases]. 821 34

We report a case of phosphate diabetes in a patient with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with sarcoidosis. Our patient was affected by systemic sarcoidosis and he fits the criteria of Schwartz for the diagnosis of SIADH. He presented with phosphate diabetes which appeared during demeclocycline (DMC) therapy and persisted for about 1 month from the end of DMC. It constitutes the fourth case of phosphate diabetes induced by tetracycline described in the literature and it is the third case of SIADH associated with sarcoidosis.
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PMID:Demeclocycline-induced phosphate diabetes in a patient with inappropriate ADH secretion and systemic sarcoidosis. 845 Sep 17


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