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)

Several classes of drugs that modify serotonin (5-HT) neurotransmission are either currently used, or are being evaluated for their potential use in the treatment of anxiety, schizophrenia, and depression. 5-HT1A agonists are considered potential anxiolytics, while some atypical antipsychotics are potent 5-HT2 antagonists (and also have modest dopamine D2 affinity). Furthermore, there is a diverse group of serotonergic drugs that may be effective antidepressants. Secretion of ACTH, corticosterone/cortisol, prolactin, renin, oxytocin and vasopressin are stimulated by activation of different 5-HT receptor subtypes, while other neurotransmitter receptors also influence the secretion of these hormones. We compared the receptor binding profiles of 5-HT anxiolytics, antipsychotics and antidepressants with their endocrine effects. These comparisons could aid in understanding both the therapeutic and side effects of these drugs.
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PMID:Endocrine and receptor pharmacology of serotonergic anxiolytics, antipsychotics and antidepressants. 135 27

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

Among patients with psychiatric disorders, especially schizophrenia, a pattern of extreme polydipsia and polyuria sometimes emerges, usually without readily identifiable medical causes. Hyponatremia may develop and progress to water intoxication, with symptoms including restlessness, confusion, seizures, or even death. We review the clinical features and pathophysiology of this syndrome and discuss nursing roles in identifying and managing patients with polydipsia and hyponatremia. While the causes of polydipsia and hyponatremia are unclear, relevant factors seem to include a possible dysfunction in central nervous system (CNS) thirst and osmoregulatory centers, the inappropriate secretion of or sensitivity to antidiuretic hormone (ADH), and psychoactive drugs. Management techniques for affected patients concentrate on careful observation, fluid restriction, and the minimization of possible exacerbating factors such as high neuroleptic dosage and cigarette consumption.
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PMID:Polydipsia and hyponatremia in psychiatric patients: challenge to creative nursing care. 235 13

Receptors for neurotransmitters can be visualized and characterized using in vitro tissue slice binding techniques and quantitative autoradiography. In this article, the general methods used in studies of this type are outlined and specific application to the study of catecholamine and neuropeptide receptors in rat and human brain tissue are described. Receptor autoradiography is used to examine regulation of dopamine receptor density in response to denervation and replacement of dopamine using brain transplants. Morphological and pharmacological aspects of vasopressin receptor ontogeny in the rat brain are examined. Finally, autoradiographic data on catecholamine receptor localization and characterization in the human hypothalamus, locus coeruleus, and frontal cortex are presented and discussed with reference to their applications in the study of neuropsychiatric disorders such as schizophrenia and senile dementia of the Alzheimer's type.
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PMID:Localization and measurement of neurotransmitter receptors in rat and human brain by quantitative autoradiography. 253 20

Elevated plasma vasopressin concentrations have been documented in antipsychotic drug-treated patients as well as a drug-free acutely psychotic patients. To evaluate the effects of antipsychotic drugs on plasma vasopressin, we measured vasopressin response to a single dose of intramuscular chlorpromazine or intravenous haloperidol in normal individuals and to 2 weeks of oral antipsychotics in patients with acute schizophrenia. Neither intramuscular chlorpromazine nor intravenous haloperidol affected plasma vasopressin in normals, except in one subject who developed high plasma vasopressin concentrations coincident with marked hypotension following chlorpromazine. Prior to antipsychotics, two acute schizophrenia patients had elevated plasma vasopressin concentrations, which normalized during antipsychotic drug treatment. We conclude that antipsychotics do not directly stimulate vasopressin release, but may indirectly stimulate vasopressin release by well-described baroreceptor reflex mechanisms if hypotension occurs. Also, acute schizophrenia may be associated with increased plasma vasopressin levels in some patients.
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PMID:Antipsychotic drugs and plasma vasopressin in normals and acute schizophrenic patients. 356 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

This article comprises a systematic ans schematic survey of neuroleptics and antidepressants, their mode of action in the central nervous system, indications and side-effects. Psychic disorders in the aged may be due to anatomical cerebral lesions, but they may be also "functional'. Both types of disorders are concisely described. The possibilities and limitations of treatment with psychotropic drugs are reviewed and special attention is given to the specific problems of this type of therapy in patients of advanced age. It is pointed out that psychic disorders in the aged are multiconditional and that psychopharmacotherapy is just one component of the treatment. The neuropeptide concept is described. The putative clinical significances of neuropeptides derived from ACTH, vasopressin and beta-endorphin (e.g. DTgammaE) are mentioned with respect to learning- and memory processes and schizophrenia.
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PMID:[Mechanism of action and indications for psychopharmaceutic agents; possibilities and limitations in the elderly]. 611 93

Although there is a definite association between hyponatremia and schizophrenia, the true incidence and etiology have not been established. This report is a retrospective study of all admissions to the Baroness Erlanger Hospital over a three and one-half year period. There was a 5.8% incidence of hyponatremia in patients with schizophrenia as compared with a 0.36% incidence for all admission (P less than .01). Schizophrenic patients at risk for developing hyponatremia drank water excessively(P less than .01) and were most likely to be taking thioxanthene (P = .05(4)) antipsychotic and anticholinergic medications (P Less than .01). Most schizophrenic patients admitted with hyponatremia had dangerously low serum sodium levels (less than or equal to 120 mEq) and showed severe neurologic dysfunction. This retrospective study compares the clinical features of schizophrenic patients who develop hyponatremia and those who do not. The possible role of antidiuretic hormone is discussed
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PMID:Hyponatremia in patients with schizophrenia. 612 72

Among the biochemical theories proposed for schizophrenia the best-founded appears to be the dopaminergic theory. Dopaminergic agonists exacerbate schizophrenic symptoms. Neuroleptics, which are the most effective drugs in schizophrenia, are dopaminergic-blocking agents. Other biochemical disorders have been demonstrated in some cases of schizophrenia but results are not always consonant. The presence of abnormal compounds, i.e. methylated derivatives or phenylethylamine, has often been mentioned. Several disorders of enzymes have also been reported, such as a defect in beta-dopamine hydroxylase or an abnormal activity of the MAO which metabolizes the indolamines and catecholamines. Disorders of the metabolism of noradrenaline and serotonin have also been suggested, mainly on experimental evidence. Other compounds have been incriminated, such as endorphins, gamma-aminobutyric acid, lysine-8 vasopressin or prostaglandins. The action of neuroleptics can be ascribed to dopaminergic respector blockade, as a safe approximation. However, the demonstration of several dopaminergic pathways and of several types of receptors makes the understanding of their mode of action all the more difficult that they interplay with many other neurotransmittors.
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PMID:[Biochemistry of schizophrenia and mechanism of action of neuroleptics]. 613 Jun 4

In Huntington's disease, there is a decrease of the neuropeptides, substance P, enkephalins, and cholecystokinin in the striatonigral system, whereas in Parkinson's disease an increase of substance P is found in the substantia nigra. Several neuropeptides should be involved in Alzheimer's disease: substance P, endorphins, vasopressin, ACTH, somatostatin, vasoactive intestinal peptide, cholecystokinin, neurotensin, delta sleep-inducing peptide. Alterations of substance P, vasoactive intestinal peptide, cholecystokinin, somatostatin, and endorphins may be related to the pathophysiology of schizophrenia. Delta sleep-inducing peptide may interfere in addiction pathology.
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PMID:Putative peptide neurotransmitters in human neuropathology: a review of topography and clinical implications. 618 57


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