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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiology behind the abnormalities of the hypothalamic pituitary adrenal cortex axis found in patients with major depressive disorder was studied by the use of the vasopressin test. The response of plasma adrenocorticotropin (ACTH) and cortisol to the injection of 10 IU lysine-vasopressin (LVP) was investigated in 18 patients meeting the DSM-III criteria for major depressive episode. The response was correlated to the outcome of the dexamethasone suppression test (DST) with the use of two different cut-off points, 139 nmol/l and 200 nmol/l respectively. The results show that no significant difference was found in ACTH or cortisol response between patients having a normal or abnormal DST. The results do not seem to support the hypothesis that the abnormalities of the hypothalamic pituitary adrenal cortex axis involve a hypersecretion of corticotropin-releasing factor (CRF) and a subsequent desensitization of the corticotrophs to CRF-stimulated ACTH release.
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PMID:Adrenocorticotropin and cortisol response to lysine vasopressin in relation to the outcome of the dexamethasone suppression test in major depressive disorder. 283 10

Two cases of delusional major depression associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) are described. Delusional depression and SIADH may both result from alterations of brain catecholamine neurotransmitters, and may coexist more commonly than previously thought. Implications for clinical practice and future research are discussed.
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PMID:Delusional depression and inappropriate antidiuretic hormone secretion. 664 2

After major depression was diagnosed in a 83-year-old woman, fluoxetine was prescribed. Six days later she became delirious and weak, necessitating hospitalization. She was found to have hyponatremia secondary to fluoxetine-induced syndrome of inappropriate antidiuretic hormone secretion (SIADH). Recovery was complete after discontinuation of the medication.
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PMID:Fluoxetine-induced SIADH: a geriatric occurrence? 845 83

A blunted thyrotropin (TSH) response is a predictor of a good response to antidepressant drug treatment in depressives and neuroleptic treatment in paraphrenic patients (Larger et al 1986). The aim of the following study was to elucidate possible relationships between different endocrine systems and to shed light on the pathogenetic hypotheses of TSH-blunting. In order to evaluate especially hypothalamic activity in severe depression we were interested in the vasopressin system as another hormonal system underlying hypothalamic control. Thirty-four patients who met the criteria for major depression according to DSM-III-R were subjected to the thyrotropin-releasing hormone (TRH) test. We also took baseline readings of the cortisol, neurophysinI (hNpI, reflecting vasopressin plasma levels), and neurophysinII (hNpII, reflecting oxytocin plasma levels) levels. Likelihood ratio tests were done with logistic regression models to analyze the phenomenon of TSH-blunting. We observed that the likelihood of a blunted TSH response increases with higher levels of hNpI and low levels of cortisol, but is unrelated to hNpII levels.
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PMID:Correlation between vasopressin baseline and TSH-blunting in depressives. 870 65

The research presented at this conference, including a series of excellent posters from junior investigators, documents the pervasive importance of affiliation and other social behaviors. Affiliative behaviors interact with, but are distinct from reproductive and aggressive behaviors. Patterns of social behaviors tend to be more species-typical than the behaviors associated with reproduction or aggression. However, neural circuits necessary for approach or avoidance also are necessary for the expression of various types of affiliative behavior such as maternal behavior or pair-bond formation. Furthermore, candidate neurochemical systems have been identified that contribute to various types of affiliative behavior. For example, studies revealing new behavioral functions for steroid hormones of the adrenal axis, such as corticosterone, and neuropeptides, including the endorphins, oxytocin and vasopressin, extend our general knowledge of neurobiology; they may also lead to studies that expand our understanding of social behavior and the connections to systems that regulate emotions. The work represented in this volume also has important implications for the study of serious neuropsychiatric disorders. For example, episodes of certain of these disorders can be induced by social stressors; in other disorders, a marked decrease in affiliative behaviors is a prominent feature of the patients' difficulties. Furthermore, abnormalities in animal systems implicated in the neurobiology of affiliation (oxytocin, vasopressin, and the hypothalamic-pituitary-adrenal system) have also been documented for major depression in humans. Animal models, such as those described at this conference, offer evolutionary perspectives, from which it is possible to extract general principles. At the same time, our understanding of the mechanistic and neurobiological substrates of both constructive and destructive social behaviors is increasing. At the conference, the evolutionary and mechanistic perspectives converged on the theme that studies of affiliative behaviors cannot be fully interpreted in isolation from other social behaviors; neither can they effectively be isolated from the biological and social contexts that shape their expression. Advances in this research area seem dependent on integrating experimental research across levels of analysis. Although this task is challenging, we are confident that an awareness of integrative principles can lead to new and important research opportunities.
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PMID:The integrative neurobiology of affiliation. Introduction. 907 40

Loss of central glucocorticoid receptor (GR) function is thought to be involved in the development of neuroendocrine and psychiatric disorders associated with corticotropin-releasing hormone (CRH) hyperactivity. The possible causal relationship between defective GR function and altered activity of CRH neurons was studied in transgenic mice (TG) expressing antisense RNA against GR. Immunocytochemical studies showed significant reductions in CRH immunoreactive neurons in the paraventricular nucleus (PVN) and in CRH and vasopressin (AVP) stores in the external zone of the median eminence. Concomitantly, stimulus-evoked CRH secretion from mediobasal hypothalami of TG mice in vitro was reduced significantly. However, CRH mRNA levels in the PVN of TG mice were marginally lower than those in wild-type (WT) mice. 125I-CRH binding autoradiography revealed no differences between WT and TG animals in any of the brain regions that were studied. Basal plasma corticosterone (cort) levels and 125I-CRH binding, CRH-R1 mRNA, POMC mRNA, and POMC hnRNA levels in the anterior pituitary gland were similar in WT and TG mice. Intraperitoneal injection of interleukin-1beta (IL-1beta) increased plasma cort levels, CRH mRNA in the PVN, and anterior pituitary POMC hnRNA similarly in WT and TG mice. The injection of saline significantly reduced anterior pituitary CRH-R1 mRNA levels in WT mice, but not in TG mice, whereas IL-1beta produced a decrease in these mRNA levels in both strains. The data show that long-term GR dysfunction can be associated with reduced activity of CRH neurons in the PVN and decreased sensitivity of pituitary CRH-R1 mRNA to stimulus-induced downregulation. Moreover, the hypothalamic changes observed in this model suggest that impaired GR function, at least if present since early embryonic life, does not necessarily result in CRH hyperexpression characteristics of disorders such as major depression.
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PMID:Reduced activity of hypothalamic corticotropin-releasing hormone neurons in transgenic mice with impaired glucocorticoid receptor function. 957 Aug 18

Hyponatremia sometimes occurs in elderly depressed patients treated wtih a serotonin reuptake inhibitor (SRI). The cause of the hyponatremia is not yet understood. The objective of this study was to determine the effects of paroxetine, an SRI, on osmoregulated release of vasopressin (also termed antidiuretic hormone) in elderly depressed patients with normal serum sodium. Four women and one man ages 61 to 74 years with a major depressive disorder were administered a water load after they had been treated with a therapeutic dose of paroxetine for 3 to 11 months. Three healthy elderly subjects not receiving paroxetine served as controls. Both the patients and the control subjects excreted > 90% of the ingested water and lowered urine osmolality to < 100 mosmol/kg. We conclude that long-term treatment with paroxetine alone does not appear to affect the ability to excrete a water load or appropriately dilute the urine during a water load (both indices of vasopressin function) in a small group of elderly patients without other risk factors for the development of hyponatremia.
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PMID:Effect of paroxetine on plasma vasopressin and water load testing in elderly individuals. 1112 62

Earlier work has shown that plasma vasopressin levels of depressed patients were higher than those of healthy controls. The aim of the present study was to determine whether plasma vasopressin levels were correlated to parameters of the circadian rhythm. Forty-one patients with major depression and twenty-five controls participated in a case-control design under natural circumstances in a field study to investigate plasma vasopressin levels three times daily, circadian motor activity, and the 24-h periodicity of body temperature for five consecutive 24-h periods. Temperature measurements consisted of at least five, but mostly six or more measurements every 24 h. Twenty-two percent of the patients, but none of the controls lacked 24-h periodicity of body temperature. In melancholic patients increased vasopressin levels in plasma correlated with a weak 24-h periodicity of body temperature. The role of vasopressin is discussed in the light of the present findings.
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PMID:Weak 24-h periodicity of body temperature and increased plasma vasopressin in melancholic depression. 1122 7

Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is one of the key biological abnormalities described in major depressive disorder, occurring in 30-50% of depressed subjects. Corticotropin-releasing hormone (CRH) and vasopressin (AVP) are the main regulators of this stress system, with the two neuropeptides acting synergistically in bringing about adrenocorticotropin (ACTH) release from the anterior pituitary and cortisol from the adrenal gland. Based on the demonstration of elevated cerebrospinal fluid levels of CRH in depressives, and other evidence, it has been postulated that excess CRH and the resultant increased HPA forward drive form the basis of neuroendocrine dysregulation in depression. However, there is an accumulating body of evidence to support a significant role for AVP in the regulation of pituitary-adrenal activity in health and also in depressive disorder. This review, based on a Medline search from 1980 to 2001, focuses on the functional neuroanatomy, receptor pharmacology, VP synergism with CRH, and the data from clinical and pre-clinical studies that support an important role for AVP in the pathophysiology of major depression. We suggest that future antidepressants may target the vasopressinergic system.
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PMID:Vasopressin as a target for antidepressant development: an assessment of the available evidence. 1220 Feb 2

The present review summarizes the findings on the role of neuropeptides in the pathophysiology of schizophrenia and major depression. Several neuropeptides as vasopressin and endorphins in particular, beta-endorphin and gamma-type endorphins, cholecystokinin (CCK), neurotensin, somatostatin and Neuropeptide Y have been implicated in schizophrenia. During the last decade, however, few attempts to explore the significance of most of these and other neuropeptides in the pathophysiology of the disease or their therapeutic potential are found in the literature. An exception is neurotensin, which exerts neuroleptic-like effects in animal studies, while CSF, brain and blood studies are inconclusive. Things are different in major depression. Here much attention is paid to the endocrine abnormalities found in this disorder in particular the increased activity of the hypothalamic-pituitary-adrenal (HPA) axis. Neuropeptides as corticotropin-releasing hormone (CRH), vasopressin and corticosteroids are implicated in the symptomatology of this disorder. As a consequence much work is going on investigating the influence of CRH and corticosteroid antagonists or inhibitors of the synthesis of corticosteroids as potential therapeutic agents. This review emphasizes the role of vasopressin in the increased activity of the HPA axis in major depression and suggests exploration of the influence of the now available non-peptidergic vasopressin orally active V1 antagonists.
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PMID:Neuropeptides involved in the pathophysiology of schizophrenia and major depression. 1275 59


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