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)

Subcutaneously (s.c.) administered [Arg8]vasopressin (AVP) potentiated seizures induced by intracerebroventricular (i.c.v.) injection of 1.95 mg pilocarpine (a muscarinic cholinergic agonist). A bell-shaped relation between dose and effect was found. I.c.v. pretreatment with a V1, V2 or oxytocin receptor antagonist was performed to determine whether and what type of receptor is involved in this proconvulsive effect of vasopressin. For these experiments a higher dose of pilocarpine (2.4 mg i.c.v.) was injected. This caused seizures in a slightly but not significantly higher percentage of the rats. A dose-dependent protective action of the V2 receptor antagonist d(CH2),[D-Ile2,Ile4]AVP (effective doses were 25 and 125 ng) on seizures was found. A reduction was observed in the number of animals that developed tonic-clonic convulsions. Neither the V1 receptor antagonist d(CH2)5[Tyr(Me)2]AVP nor the oxytocin receptor antagonist desGly(NH2)9d(CH2)5[Tyr(Me)2Thr4]OVT possessed anti-convulsive activity. Subsequently the type of receptor was studied in detail with fragments of AVP with either V1 or V2 activity. AVP (with V1 and V2 affinity) (1 and 3 microg s.c.) potentiated pilocarpine (1.95 mg) induced seizures. Vasotocin and oxytocin were without effect. Interestingly neither s.c. nor i.c.v. administration of the selective kidney type vasopressin receptor (V2) agonist dDAVP potentiated pilocarpine induced seizures. Several selective antidiuretic agonists (V2), such as d[Val4]AVP, d[Phe2,Val4,D-Arg8]vasopressin (3 microg), [Val4,D-Arg8]vasopressin (3 microg) and d[Val4,D-Arg8]vasopressin (3 microg) were active. Other selective antidiuretic compounds, such as [Val4]AVP, dAVP, d[Tyr(Me)2]AVP and HO[D-Arg8]vasopressin (3 microg) did not influence seizures. These results demonstrate that a combination of substitution of aminoacid 4 (Gln) by Val and to a lesser extent deamination and the D-arginine form yield an active molecule, which can potentiate pilocarpine induced seizures and suggest the existence of a V2 receptor subtype in the brain.
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PMID:Proconvulsive effect of vasopressin; mediation by a putative V2 receptor subtype in the central nervous system. 921 58

The alpha2-adrenergic agonist clonidine and the neuropeptide oxytocin, inhibit sodium intake when injected intracerebroventricularly (i.c.v.). The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. injection of idazoxan, an alpha2-adrenergic antagonist. Clonidine (30 nmol), oxytocin (40, 80 nmol) and vasopressin (40, 80 nmol) were injected i.c.v. 20 min prior to a 1.5% NaCl appetite test, in rats depleted of sodium for 24 h by a combination of a single s.c. injection of furosemide (10 mg/rat) and removal of ambient sodium. Every dose of clonidine, oxytocin and vasopressin inhibited the 1.5% NaCl intake. Seizures were observed with the higher dose of vasopressin, but not with either dose of oxytocin. The effect of i.c.v. injection of clonidine (30 nmol), oxytocin (80 nmol) or vasopressin (40 nmol) was partially inhibited by prior i.c.v. injection of idazoxan (160, 320 nmol). The results suggest that the inhibition of 1.5% NaCl intake induced by i.c.v. injection of neuropeptides in sodium-depleted rats depends, in part, on the activation of central alpha2-adrenoceptors.
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PMID:Idazoxan and the effect of intracerebroventricular oxytocin or vasopressin on sodium intake of sodium-depleted rats. 922 97

Reliable observation of ECT-induced hormone release requires that other processes that affect hormone levels remain constant and not obscure it. This article reviews principles and pitfalls in making such observations. Clinical applicability and limitations of measurements of prolactin, cortisol, oxytocin, vasopressin, and other hormones are described. Applications include elucidation of ECT physiology and seizure quality, comparison of ECT techniques, and description of illness severity. Accounting for each of these different effects can be needed to characterize any of them. An important but unrealized application of neuroendocrine measurement is prediction of the stability of individual ECT response.
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PMID:Neuroendocrine effects of electroconvulsive therapy (ECT). 923 Jun 41

A 48 year-old white male not suffering from endocrine disease or polydipsia, not taking diuretics, and suffering from no renal disease was started on risperidone and discharged on no other drug from Western Missiouri Mental Health Center (WMMHC) after an 8-day hospitalization. Seven days later he was admitted to a university medical center with generalized seizures, hyponatremia, respiratory failure, and rhabdomyalysis. He eventually recovered, was transferred back to WMMHC, and stabilized on appropriate medication. A search of the literature indicates no case reports linking risperidone to hyponatremia. It is assumed that the mechanism of hyponatremia is similar to other psychotropic medication in that it is secondary to the syndrome of inappropriate antidiuretic hormone (SIADH).
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PMID:Risperidone and hyponatremia: a case report. 933 85

Adverse effects associated with antidepressant drug therapy rarely cause significant morbidity or mortality. Nevertheless, the successful management of patients with depression requires recognition of potential adverse effects that have serious consequences, which include the discontinuation of otherwise effective therapy. The aim of this overview is to highlight the more common and potentially deleterious adverse effects of both older and newer classes of antidepressant drugs. Major adverse effects attributed to the tricyclic antidepressant drugs (TCAs) include conduction defects and lethal overdose. Most worrisome with the selective serotonin reuptake inhibitor drugs (SSRIs) is the serotonin syndrome. Although rare, this syndrome can be insidious and lethal. Recent trends toward the use of medication combinations and augmentation therapies significantly enhance the risk of serotonin syndrome. Cognitive impairment also may occur, especially with the TCAs. Apathy is occasionally a problem with SSRI therapy. The syndrome of inappropriate antidiuretic hormone (SIADH) has been reported with most antidepressant drugs but appears to be more common with serotonergic agents and in elderly patients. Although seizures are uncommon in patients receiving antidepressant therapy, the risk must be understood by both the patient and the clinician. Adverse effects related to sexual function are common, especially with TCAs, SSRIs, and venlafaxine. Sexual dysfunction often leads to noncompliance and self-discontinuation of therapy. Sleep disturbances are common in patients with depression, and recent data illustrate how crucial sleep regulation is to mood. Antidepressant drugs vary in their sleep effects. Although antidepressant drugs can cause a variety of adverse effects, these drugs save lives and their benefits far exceed their risks.
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PMID:Antidepressant drugs: disturbing and potentially dangerous adverse effects. 979 63

The spread of experimentally kindled seizures in rats results in sustained increases in plasma vasopressin (VP) and VP mRNA in the supraoptic nucleus (SON). These increases provide an excellent example of the pathological plasticity that can develop in normal cells exposed to recurrent seizure activity. To test whether this plasticity might be due in part to changes in metabotropic glutamate receptors (mGluRs), we examined mGluR mRNA expression in the SON 1 month after stage 5 amygdala kindling. Three mGluR subtypes were detected by in situ hybridization in the SON in the following relative levels: mGluR3 > mGluR1 > mGluR7. Both mGluR1 and mGluR3 mRNAs were significantly increased in the SON (+28-61%) and cortex (+27-42%) after kindling. Immunoreactivity for mGluR1 but not mGluR2/3 was significantly increased in vivo in the SON. Receptor protein expression and intracellular calcium accumulation in response to the mGluR agonist, 1S,3R ACPD, were evaluated after in vitro "kindling" of neuroendocrine cells by Mg2+ deprivation. Increased immunoreactivity for mGluR1 and mGluR2/3 was seen in all cultures 3 days after a brief exposure to Mg2+-free medium. 1S,3R 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) induced rapid peak responses and gradual accumulations of intracellular Ca2+ in neurons. Both responses were increased in the "kindled" cells. Increases in the expression of functional mGluR1 and perhaps mGluR3 receptors may contribute to the development of long-lasting plastic changes associated with seizure activity.
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PMID:Kindled seizures increase metabotropic glutamate receptor expression and function in the rat supraoptic nucleus. 981 46

Psychotropic drugs, as well as some psychiatric disorders, can produce neurotoxic and life-threatening abnormalities of water and electrolyte balance that require prompt and appropriate medical intervention. Compulsive fluid intake by psychotic patients (primary polydipsia) can produce delirium due to water intoxication with hyponatremia. Several psychotropic drugs cause water retention by decreasing renal clearance, as in the syndrome of inappropriate antidiuretic hormone secretion. Lithium and other agents interfere with renal resorption of water to cause nephrogenic diabetes insipidus. Clinical signs in these disorders range from lethargy and confusion to stupor, seizures, coma, and death. This overview provides a conceptual framework for differentiating among and safely managing these relatively common disorders.
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PMID:Primary and drug-induced disorders of water homeostasis in psychiatric patients: principles of diagnosis and management. 1037 Apr 44

Modern data of molecular and biological properties and physiological role of new pituitary adenylate cyclase activating polypeptide--PACAP--review. PACAP play key role in the embryogenesis of brain, in the protection of brain nerve cells from ischemia-induced death, injuring and apoptosis. New data are discussed concerned with molecular cloning and tissue distribution of receptors for PACAP, gene proPACAP expression in gastrointestinal tract, reproductive organs and nervous system. PACAP increase cytosolic free calcium and modifies the calcium-sensitive K(+)-channels, PACAP protects cultures cortical and hippocampal neurons from glutamate-induced cytotoxicity. The sleep modulation and modification of seizures activity of brain through the secretion of vasopressin or/and through NMDA receptors directly should be include in the program of PACAP "physiological continuum" of functions.
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PMID:[Pituitary adenylate cyclase activating peptide (PACAP)--its polyfunctionality in the mechanisms of brain protection]. 1042 Apr 72

Neuropeptides are peptides which affect the nervous system. They are derived from large precursor molecules. These are converted to neurohormones, neuropeptides of the "first generation", which can be further converted to neuropeptides of the "second generation". This review is a brief survey of the nervous system effects of neuropeptides derived from pro-opiomelanocortin (POMC) and the neurohypophyseal hormones. Processing of these molecules results in neuropeptides of the first and second generation which have similar, different, more selective or even opposite effects. Among those are effects on learning and memory processes, grooming, stretching and yawning, social, sexual and rewarded behavior, aging and nerve regeneration, thermoregulation, pain, sensitivity to seizures, and cardiovascular control. Results of animal studies as well as those of clinical studies suggest that these neuropeptides may be beneficial in aging, neuropathy, memory disturbances and schizophrenia. Most of these nervous system effects in animal studies were found before receptors in the nervous system for the various neuropeptides were detected. G-protein-coupled receptors for the neuropeptides of the "first generation", i.e., melanocortin receptors, opioid receptors, and neurohypophyseal hormone receptors have been found, in contrast to the receptors for neuropeptides of the "second generation", although there are indications that G-protein coupled receptors for these may be present in the brain.
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PMID:Behavioral pharmacology of neuropeptides related to melanocortins and the neurohypophyseal hormones. 1044 60

Electroconvulsive therapy (ECT) is known to stimulate subcortical brain regions and release hormones from the anterior and the posterior pituitary. To enhance the subcortical effect of ECT and the neuroendocrinological response we used high dose right unilateral ECT (RUL-ECT) in 11 depressive patients and studied its effect on the release of vasopressin, prolactin and neuropeptide FF. The RUL ECT stimulus for all studied patients was 5 times the individual seizure threshold and it led to immediate release of vasopressin in all studied patients. The release of prolactin was less uniform however in accordance with results from earlier studies. The ECT also stimulated a NPFF secretion peak that came approximately 5 min after ECT stimulus and preceded the prolactin peak. The maximal elevations in circulating vasopressin and prolactin concentrations were 680% and 950%, respectively. The neuropeptide FF concentration increased by 100% after ECT. There was a second rise in NPFF concentration at 25 min after the ECT treatment. The increases in all peptide concentrations were significant, but were not correlated with each other. The neuropeptide FF concentration returned to baseline level at 10 min and the vasopressin concentration at 25 min after ECT. The prolactin concentration remained increased during the 30 min follow up period. Our results complete earlier finding on ECT stimulated vasopressin and prolactin release and show that high intensity RUL-ECT releases neuropeptide FF into human blood. The modest rise of circulating NFFF most likely represents leakage from the CNS.
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PMID:Blood concentrations of vasopressin, neuropeptide FF and prolactin are increased by high-dose right unilateral ECT. 1044 89


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