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)

Intracerebroventricular (i.v.t.) administration of beta-endorphin or leucine5-enkephalin inhibited drinking behavior, the pressor response and increased plasma vasopressin concentration stimulated by an acute elevation in CSF sodium chloride concentration (10 microliter, 1 M NaCl i.v.t.). These effects of endogenous opioid peptides were prevented by naloxone, indicating opiate receptors were required for the biologic response. Drinking behavior associated with regulatory stimuli operant during dehydration was also inhibited by opioid peptides. beta-Endorphin (i.v.t.) delayed the onset and/or reduced the volume of water consumed in response to hypertonic sodium chloride (relative cellular dehydration), polyethylene glycol (hypovolemia) and food-associated drinking behavior. Inhibition of drinking did not appear related to sensory-motor dysfunction as another motivated behavior, eating (onset, amount consumed) was unaffected by beta-endorphin. It is concluded from these results that centrally administered endogenous opioid peptides inhibit sodium chloride-stimulated cerebral mechanisms affecting blood pressure and hydration.
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PMID:Effects of centrally administered endogenous opioid peptides on drinking behavior, increased plasma vasopressin concentration and pressor response to hypertonic sodium chloride. 626 92

In 13 patients suffering from renal dysfunction and treated by chronic haemodialysis, the mnemic functions appeared within the limits of normality and there was no positive correlation between blood levels of neurophysines and free cortisol. On the other hand, a negative correlation was found between levels of neurophysine I and items 3 and 5 of the memory test PRM. This negative result indicates that in haemodialyzed patients a discrepancy may exist between blood levels of neurophysines and vasopressin release, or that there is no direct relationship between plasma and CSF concentrations of such hormones.
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PMID:A study of psychological and endocrine variables on 14 patients treated by chronical haemodialysis. 627 63

A patient with non-Hodgkin's lymphoma who was previously treated with chemotherapy and radiotherapy was seen with intestinal pseudoobstruction due to paralytic ileus associated with herpes zoster (varicella zoster) infection. The infection was accompanied by a polydermatomal rash with typical morphologic characteristics, followed by cutaneous dissemination and the syndrome of inappropriate antidiuretic hormone (SIADH), as well as myotomal paresis. The diagnosis was supported by cytology and by culture of the virus from the CSF. The isolation of the virus from the CSF, coupled with abnormalities of the patient's mental status and CSF, indicate that meningoencephalitis occurred and probably accounted for the SIADH. The patient had a spontaneous and complete recovery. To our knowledge, this is the first report of SIADH associated with herpes zoster infection.
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PMID:Disseminated varicella-zoster virus infection with the syndrome of inappropriate antidiuretic hormone. 630 97

Injection of insulin to the CSF in the presence of spontaneous diuresis and hydration gives rise to the growth of reabsorption of osmotically free water accompanied by high tubular transport, as well as to the development of antinatriuresis and inhibition of diuresis. Experiments with a preliminary blockade of beta-adrenoreceptors with propranolol or administration of a beta-blocker following insulin injection demonstrated beta-adrenoreactive brain structures to be involved in the mechanism of action of insulin. Secondary activation of vasopressin secretion and release in the blood may be mediated via these structures, as a result of which reabsorption of osmotically free water in renal tubules gets increased. Thus, CSF insulin effects its influence on renal function via the central neurohumoral mechanisms which work due to beta-adrenergic brain receptors.
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PMID:[Mechanism of the central action of insulin on kidney function]. 631 56

We studied the concentration of neurophysin I (hNPI) and II (hNPII), the hypothalamo-pituitary carriers of vasopressin and oxytocin, in CSF of depressed and schizophrenic patients and age matched controls. Mean hNPI values were lower and mean hNPII values greater in schizophrenics than in controls. Lower hNPI values were observed in unipolar patients than in controls. In bipolar patients however, higher hNPI values were present. Significantly higher hNPII values were observed in bipolar patients than in controls; no difference was present between unipolars and controls. A positive correlation was observed with age in controls and bipolars for hNPII. These data emphasize the interest of studying the neurohypophysal function in affective illness and in schizophrenia.
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PMID:Cerebrospinal fluid neurophysins in affective illness and in schizophrenia. 648 3

A recently developed small controlled-delivery peptide device has now been further miniaturized (3.5 mm3 rod) and its action has been tested in vitro and in vivo using vasopressin (VP) as experimental substance. In vitro immersion showed a constant and lasting release of VP for weeks, as had been described for larger devices. By introducing the mini-device into the lateral ventricle of rat brain and by sampling CSF via a permanent cannula in the cisterna magna, a steadily enhanced level of VP could be attained for CSF. These increased levels persisted for one week, but most likely continue for longer periods.
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PMID:Successful ventricular application of the miniaturized controlled-delivery Accurel technique for sustained enhancement of cerebrospinal fluid peptide levels in the rat. 651 86

Plasma and CSF 1-desamino-8-D-arginine-vasopressin (DDAVP) levels were measured by radioimmunoassay following the infusion at constant rates of various amounts of DDAVP (12.5-20 ng/kg/min) into the jugular veins of 4 adult sheep prepared with chronic, indwelling cisterna magnum catheters, as well as jugular vein and carotid artery catheters. The mean steady-state CSF DDAVP concentration did not vary significantly from zero. Thus, DDAVP does not cross the blood-CSF barrier when administered intravenously.
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PMID:Does DDAVP (1-desamino-8-D-arginine-vasopressin) cross the blood-CSF barrier? 663 16

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 content of vasopressin (AVP) and oxytocin (OXT) in the septum, hippocampus, hypothalamus and cortex was determined at 5 min and 24 hr after peripheral (intraperitoneal) administration of histamine (20.0 mg/kg) and pentylenetetrazol (45.0 mg/kg) and in the cerebrospinal fluid at 24 hr after pentylenetetrazol treatment. At 5 min after administration of histamine the AVP content in the septum was increased whereas the OXT level in the various areas was not changed. At 24 hr, neurohypophyseal peptide contents were unaffected in the brain regions analyzed. Pentylenetetrazol did not alter AVP content at 5 min after its administration, however, the OXT level in the septum and the cortex was diminished. At 24 hr after administration of pentylenetetrazol a decreased AVP content in the hippocampus and in the cortex was observed. In contrast, OXT content in the cortex was increased at this time. AVP and OXT levels in CSF were not changed at 24 hr following pentylenetetrazol treatment. The present results suggest that the levels of neurohypophyseal hormones can be differentially altered in particular brain regions at short- (5 min) and long- (24 hr) term intervals after treatment with histamine or pentylenetetrazol. Long-term changes in AVP and OXT levels after pentylenetetrazol may be implicated in the amnesic properties of this convulsive drug. Furthermore, the present findings point to a possible relationship with previously reported pentylenetetrazol-induced changes in peptide levels in the CSF.
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PMID:Vasopressin and oxytocin content in cerebrospinal fluid and in various brain areas after administration of histamine and pentylenetetrazol. 664 96

Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. We injected various doses of saralasin into a lateral cerebroventricle (IVT) of conscious, male rats deprived of water for 48 h and killed them at different times. The concentration of AVP in the plasma (p[AVP]), measured by radioimmunoassay, was unaffected by saralasin. IVT pretreatment with 1-Sar-8-Ile-angiotensin II blocked maximal AVP release by IVT angiotensin, but this pretreatment did not reduce p[AVP] after 24, 48 or 72 h water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 micrograms/h) into 48-hour water-deprived rats revealed equivalent p[AVP] and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (a) drank at similar rates, (b) excreted similar amounts of urine, and (c) reduced their p[AVP] levels to the same extent. IVT saralasin did not affect p[AVP] of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p[AVP] of 48-hour water deprived rats about 30% (p less than 0.05). We conclude that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.
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PMID:Vasopressin release induced by water deprivation: effects of centrally administered saralasin. 665 1


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