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)

The neuropeptides vasopressin (AVP) and oxytocin (OXT) are supposed to be involved not only in peripheral functions (e.g. diuresis, labour and lactation) but also in central processes that are frequently disturbed during aging and senile dementia (e.g. fluid and electrolyte homeostasis and cognitive functions). A concomitant decrease in activity of the hypothalamo-neurohypophyseal system (HNS) with aging has been postulated in the literature, but has not yet been established. In order to investigate possible age-related changes in the human HNS, immunocytochemically identified AVP and OXT neurons in the paraventricular and supraoptic nucleus (PVN and SON) were analysed morphometrically in subjects from 10 to 93 years of age, including patients with senile dementia of the Alzheimer type (SDAT). Cell size was used as a parameter for peptide production. Mean profile area of OXT cells did not show any significant changes with increasing age. Mean profile area of AVP cells, however, showed an initial decrease up to the sixth decade of life, after which a gradual increase was observed. Size of AVP and OXT cell nuclei did not change significantly with aging. Observations in brains from patients with SDAT were within the range for their age group. The present results do not support degeneration or diminished function of the HNS in senescence or SDAT, as generally presumed in the literature, but suggest an activation of AVP cells after 80 years of age. The activation of AVP cells in senescence is in accordance with previous findings in the aged Wistar rat.
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PMID:The vasopressin and oxytocin neurons in the human supraoptic and paraventricular nucleus; changes with aging and in senile dementia. 404 17

Changes in the activity of neurotransmitters in dementia were studied by measuring the activities of each of choline acetyltransferase (CAT), dopamine-beta-hydroxylase (DBH) and hydroxylase cofactor (tetrahydrobiopterine; BPH4), and the concentrations of homovanillic acid (HVA) and vasopressin. CAT activity was low in the cerebral cortex of patients with senile dementia of Alzheimer's type (SDAT). The CAT activity was high in the nucleus basalis, which correlated well with the CAT activity in the cerebral cortex, Brodmann areas 22 and 17. DBH activity was lower in the cerebrospinal fluid (CSF) of SDAT and multi-infarct dementia (MID) patients than in that of control subjects. No age-related change was observed in control subjects. Serum DBH activity was decreased in patients with SDAT but not in patients with MID. DBH activity was especially low in the serum of SDAT patients with a low dementia rating score and/or severe brain atrophy shown on computed tomography (CT) scan. Serum DBH activity was also decreased in older normal subjects (greater than or equal to 80 years). The concentration of HVA in the CSF of control subjects decreased with the advance of age, but the decrease in HVA concentration was more pronounced in the CSF of SDAT patients, which would reflect the lowered dopaminergic activity in SDAT. BPH4 activity was also decreased in the CSF of SDAT patients. Arginine-vasopressin was widely demonstrated in the cerebral cortex of control subjects but could not be detected in many areas of the cerebral cortices of demented patients. These results suggest that a deficit of dopamine, noradrenaline or vasopressin as well as acetylcholine may occur in the brain of SDAT patients. The evidence presented points toward areas for consideration in the search for methods of therapy or prevention of SDAT.
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PMID:Neurotransmitters in dementia. 615 97

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

Many of the neurochemical changes associated with aging brain, particularly lower choline acetyltransferase and higher monoamine oxidase, occur with greater severity in senile dementia, Alzheimer's type (SDAT). These alterations correlate with neuropathologic indices, e.g., the number of senile plaques and tangles. Although many different treatment techniques have been used, most have been unsuccessful. No strong data have supported the use of stimulants, Gerovital H3, or hyperbaric oxygen. Among the vasodilators, cyclandelate and hydergine may be of value in some but not most patients. Much recent work has focused on techniques to increase acetylcholine brain concentrations. To date, precursors, such as choline, seem to have very limited value. Postsynaptic treatments, e.g., physostigmine, hold more hope for future benefit, if longer acting oral preparations are developed. Other compounds, such as ACTH, vasopressin, and piracetam, may have some value but need better definition and treatment indications. Recent discoveries on the influences of lecithin on membrane fluidity and receptor binding, may affect the focus of future pharmacologic investigation.
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PMID:Chemotherapy of cognitive disorders in geriatric subjects. 632 57

Alzheimer's disease is an insidious degenerative disease of the brain and is the leading cause of dementia in the U.S. Numerous etiologies have been postulated, including a large body of evidence suggesting a slow viral infection, possibly in genetically predisposed individuals, but this remains to be proven. Differential diagnosis is based primarily on exclusion of other treatable forms of dementia. Neurochemical studies suggest a cholinergic deficit; thus primary emphasis in treatment has been directed at enhancing cholinergic activity. Choline and lecithin supplementation generally has been ineffective. Results with physostigmine are encouraging and further studies with this drug prototype are needed. Physostigmine's clinical usefulness is limited, however, due to peripheral side effects and its short duration of action. Other pharmacological approaches, such as naloxone, neural metabolic enhancers, stimulants, and vasopressin analogs, have been investigated. The clinical features and pathology of the disease are reviewed.
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PMID:Alzheimer's disease: clinical features, pathogenesis, and treatment. 638 52

In 16 patients with primary degenerative dementia mean CSF vasopressin concentration was lower (0.9 +/- 0.1 pg/ml (mean +/- SEM)) than in 28 control patients (1.3 +/- 0.1 (mean +/- SEM)) (p less than 0.01). In 18 patients with normal pressure hydrocephalus and potentially reversible dementia mean CSF vasopressin concentration (1.2 pg/ml +/- 0.1 (mean +/- SEM)) was not different from that found in controls. Several of the demented patients had inappropriate plasma vasopressin concentrations suggesting a defect in osmoregulation. These findings encourage further clinical trials of vasopressin in patients with primary degenerative dementia, but it is emphasised that the low CSF vasopressin concentration in these patients might be only a nonspecific phenomenon due to the diffuse loss of cells within the central nervous system.
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PMID:CSF and plasma vasopressin concentrations in dementia. 664 15

The effects of lysine vasopressin on memory and cognitive deficits in Alzheimer disease was investigated. In a double-blind study, seven patients were given 16 units of lysine vasopressin per day for 10 days and were compared with seven different patients receiving placebo. No significant difference in performance between the vasopressin and placebo-treated groups was found in tests designed to evaluate learning, memory, and perception. However, significantly greater improvement in reaction time was seen in the vasopressin-treated group, although this effect was delayed and may have been contributed to by factors other than drug activity.
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PMID:Lysine vasopressin in Alzheimer disease. 720 Nov

Aging, as well as some frequently associated pathological conditions (depression, dementia, Alzheimer's disease, etc.), has been shown to have a profound impact on the normal functioning of the hippocampus-hypothalamo-pituitary-adrenocortical axis system. The hypothalamo-pituitary-adrenocortical axis in the aged rat is characterized by an increase in the basal level of circulating corticosterone, an impaired ability to recover from the adrenocortical stress response, and a reduced sensitivity to the dexamethasone suppression test. All these alterations may arise from a reduced hippocampal negative feedback control of the axis, as suggested by the age-dependent loss of hippocampal adrenocorticoid receptors. Among the hypothalamic corticotropin secretagogues, corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP) are considered the main physiological mediators of hypothalamic control of ACTH release. Thus, we have investigated the dynamic and the temporal course of the adrenocortical response to CRH and AVP in the aged rat. Freely moving jugular-catheterized male Sprague-Dawley rats (3- and 24-month-old) were injected with CRH (0.5, 0.05 and 0.01 microgram/kg i.v.), or AVP (1.0, 0.1 and 0.05 microgram/kg i.v.), or CRH and AVP in combination. In addition, adrenocortical sensitivity to corticotropin has been studied by injecting ACTH (10 ng/kg i.v.). Our study has (1) indicated that the response to ACTH secretagogues is dampened with aging, and (2) shown in the aged rat a slower recovery. Moreover, the results had confirmed the age-dependent increase in the basal level of corticosterone in the rat, and shown no age-related differences in the glucocorticoid response to ACTH.
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PMID:Reduced glucocorticoid response to corticotropin secretagogues in the aged Sprague-Dawley rat. 756 36

The total number of immunocytochemically identified vasopressin (AVP) cells was determined morphometrically in the paraventricular (PVN) and dorsolateral part of the supraoptic nucleus (dl-SON) of the human hypothalamus in 30 subjects ranging in age from 15 to 97 years, including 10 Alzheimer's disease (AD) patients. The aim of the present study was to test the hypothesis that the increased activity of AVP neurons reported earlier is accompanied by an absence of cell loss in these nuclei in senescence and AD. The results show that numbers of immunoreactive AVP cells in the PVN and dl-SON do not decline during aging or in AD. During aging, the number of neurons expressing AVP even increased in the PVN of control subjects. The nuclear diameter of the AVP cells in the PVN and dl-SON showed an increase in old AD patients. It is concluded that no cell loss occurs in the AVP cell population in the PVN and dl-SON during aging and in AD, and that AVP expression increases in the PVN during normal aging, but not in AD.
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PMID:No vasopressin cell loss in the human hypothalamus in aging and Alzheimer's disease. 772 30

Change in calcium response was studied to clarify the pathological process of Alzheimer's disease (AD). Cultured fibroblasts from patients with familial Alzheimer's disease (FAD; n = 6), sporadic Alzheimer's disease (SAD; n = 4), and age-matched healthy control subjects (n = 4) were studied with an ACAS Interactive Laser Cytometer (ACAS-470). Fibroblasts from two independent families with FAD (OS-1, and OS-2 families) showed a suppressed calcium response after stimulation by 100 nM bradykinin (BK) 100 nM vasopressin (VP) or 10% FCS in Ca(2+)-free condition compared with control fibroblasts at 48 h after plating. However, on the 7th day after plating, the abnormal calcium response was no longer observed. The height of the calcium peak showed periodic variation, indicating a relationship of calcium response with the cell cycle. When fibroblasts from OS-1 and OS-2 families were arrested in S phase, they showed a significantly suppressed calcium peak after BK stimulation. However, when those fibroblasts were arrested in other phases, they showed the same calcium peak as the other cells. The suppression of calcium response in S phase was indistinguishable from the calcium suppression induced by A23187 administration. Since Hardy type mutation on amyloid precursor protein gene is found in the OS-1 family, the observed abnormalities in calcium response might be related with pathological processing of amyloid precursor protein in AD. The reported abnormal calcium response, which is observed most obviously in fibroblasts in S phase, may indicate participation of the cell-cycle-dependent process in the pathology of AD.
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PMID:Cell-cycle-dependent abnormal calcium response in fibroblasts from patients with familial Alzheimer's disease. 772 21


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