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)

Animal studies have revealed two important aspects of vasopressin function which make this peptide a suitable candidate for involvement in complex behavioural syndromes: (1) vasopressin deficiency produces deficits of behaviour which are reversed by vasopressin; (2) well-developed systems exist for the distribution of vasopressin throughout the central nervous system (C.N.S.) via either peptidergic neurons or the cerebrospinal fluid (C.S.F.) and provide the means by which vasopressin may regulate cells controlling behavioural or physiological processes. Among the processes which vasopressin can influence are several of significance in the symptom-complex of affective illness, including alterations in memory, changes in pain sensitivity, synchronisation of biological rhythms, the timing and quality of R.E.M. sleep, and the regulation of fluid and electrolyte balance. In addition, vasopressin is functionally linked to monoamine neurotransmitter systems and, like them, is altered by pharmacological agents which affect mood. Some of the pharmacological and clinical data suggest that vasopressin function is diminished in depression and augmented in mania; sometimes, however, alterations in vasopressin function may be detectable only during crucial periods of the manic-depressive cycle. The hypothesis that vasopressin plays a role in disorders of human behaviour, particularly manic-depressive illness, can now be directly tested by radioimmunoassays of vasopressin in C.S.F. and plasma and by the administration of specific vasopressin analogues and inhibitors.
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PMID:Vasopressin in affective illness. 7 97

Neurophysins are neuropeptides (MW +/- 10,000) synthetized together with active nonapeptides vasopressin (AVP) and oxytocin (OT). The original description of the radioimmunoassay for neurophysins in 1969 allowed us to demonstrate the concomitant, equimolecular, release of them together with AVP and OT, thus bringing strong arguments in favour of neurohypophyseal exocytosis. Beside the use of those RIAs as direct indexes of neurohypophyseal release in various physiological and pathological conditions, we have been interested these last two years, to the putative use of neurophysins RIA as direct neuroendocrine markers in various neuropsychiatric diseases (depression, mania, schizophrenia) and paraneoplastic syndromes (SIADH).
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PMID:[Neurophysins]. 209 28

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
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PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

Cerebrospinal fluid (CSF), thyrotropin releasing hormone (TRH), CSF-vasopressin (AVP), plasma-AVP, CSF-osmolality, plasma-osmolality, CSF-adrenaline (A) and -noradrenaline (NA) were measured in psychiatric patients and controls. Psychiatric patients were classified according to ICD-9 and grouped into endogenous depression, non-endogenous depression, mania and schizophrenia. The depressive groups were classified according to the Newcastle Rating Scale for Depression 1965. Severity of disease was quantified by BRMES, BRMS and BPRS. No difference in CSF-TRH levels was seen among the different diagnostic groups and controls. A positive correlation between CSF-TRH and CSF-A was demonstrated. CSF-AVP concentrations were significantly lowered in both endogenous and non-endogenous depression; no correlation with CSF-A or -NA was seen. Neither did any difference between plasma levels of AVP, plasma-osmolality or CSF-osmolality appear among the groups investigated.
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PMID:Cerebrospinal fluid vasopressin--changes in depression. 393 7

Since the approval of lithium use in treatment of acute mania, there have been numerous clinical trials of lithium in medical and psychiatric disorders. This paper gives a brief review of the literature on lithium trials in approximately fourteen medical conditions. These are: hyperthyroidism, metabolizing thyroid cancer, syndrome of inappropriate secretion of antidiuretic hormone, premenstrual tension syndrome, anorexia nervosa, Felty's syndrome, chemotherapy-induced neutropenia, aplastic anemia, seborrheic dermatitis, eczematoid dermatitis, cyclic vomiting, diabetes mellitus and asthma. Most of the case reports cited showed the efficacy of the side effects from lithium salt in the management of the symptoms and signs of these disorders, however, well-designed and controlled studies give negative results. The positive results are reported in the group of disorders having an underlying subdromal affective syndrome such as premenstrual tension syndrome and anorexia nervosa. Other encouraging reports include the effect of lithium to induce leucocytosis in Felty's syndrome and chemotherapy-induced neutropenia.
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PMID:A review of clinical trials of lithium in medicine. 639 35

This overview summarizes the major and minor side effects and drug interactions of fluoxetine. The adverse reactions include the "serotonin syndrome", cardiovascular complications, extrapyramidal side effects such as akathisia, dyskinesias, and parkinsonian-like syndromes and an apparently increased risk of suicidality. Fluoxetine-induced mania and hypomania, seizures and sexual disorders are evaluated along with minor symptoms of allergic reactions, stuttering, hematological changes, psoriasis, and inappropriate secretion of the antidiuretic hormone. The major fluoxetine-drug interactions involve the amino acids L-dopa and L-tryptophan, anorexiants, anticonvulsants, antidepressants, anxiolytics, calcium channel blockers, cyproheptadine, lithium salts, and drugs of abuse. The underlying mechanism and the paradoxical effects of fluoxetine are addressed.
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PMID:Fluoxetine: adverse effects and drug-drug interactions. 825 2

Recurrent manic-like episodes can be induced by hyponatremia possibly due to empty sella syndrome. In the present case, the patient was proven to have syndrome of inappropriate antidiuretic hormone (SIADH) secretion with manic symptoms that resolved after the normalization of the plasma sodium level.To our knowledge, this is the first case of hyponatremia-induced manic symptoms in a patient with empty sella syndrome. More attention should be paid to late-onset mania, because it may be the sign of a more serious medical problem.
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PMID:A Case Report of Late Onset Mania Caused by Hyponatremia in a Patient With Empty Sella Syndrome. 2687 84