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)

To assess the penetration of desglycinamide-arginine-vasopressin (DGAVP, Org 5667) to the central nervous system, levels of DGAVP were measured in the lumbar CSF after peripheral administration. DGAVP (2 mg) was administered intranasally to 37 patients and CSF samples were collected from these patients 5 to 240 minutes later. Detectable levels of DGAVP in CSF could be found 5 minutes after administration, but levels declined rapidly during the next 90 minutes. The DGAVP levels in CSF correlated with plasma levels of DGAVP (r=0.586, p less than 0.001). According to these results, DGAVP may gain access to the central nervous system and may induce central effects.
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PMID:Penetration of DGAVP (Org 5667) across the blood-brain barrier in human subjects. 358 46

CSF vasopressin levels were significantly elevated in eight patients with motor neuron disease (2.5 +/- 0.4 pmol/l) compared with controls (0.7 +/- 0.1 pmol/l). CSF oxytocin and plasma vasopressin concentrations were similar in the two groups. This finding may be a primary part of the disease process or an epiphenomenon related to increased autonomic and descending pathway activity secondary to abnormal function and/or loss of anterior horn cells.
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PMID:Elevated cerebrospinal fluid vasopressin in motor neuron disease. 361 58

Endogenous opioid peptides inhibit secretion of oxytocin during dehydration, hemorrhage and parturition and attenuate release of vasopressin by tail electroshock. Diverse agents were used to stimulate the hypothalamo-neurohypophysial system to investigate the hypothesis that if oxytocin (or vasopressin) release were inhibited by opioid peptides regardless of the stimulus, the site of opiate action may be in the final common pathway (i.e. the magnocellular neuron) or on pituicytes in the neural lobe. Using male Sprague-Dawley rats, we therefore investigated the effect of an opiate receptor antagonist, naloxone (5 mg/kg s.c.), on the plasma concentrations of oxytocin and vasopressin elevated by various pharmacologic stimuli, including histamine (10 mg/kg i.p.), nicotine (0.15 or 1.5 mg/kg i.p.), isoproterenol (30 or 120 micrograms/kg i.m.) and increased [NaCl] in cerebrospinal fluid (CSF; 10 microliter artificial CSF containing 1 M NaCl i.v.t.). Control animals received saline (0.85%) or artificial CSF (containing 0.16 M NaCl). Animals were decapitated 60 s (increases[NaCl] in CSF) or 10 min after the stimulus or vehicle. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. The concentrations of oxytocin and vasopressin in plasma were elevated (p less than 0.05) by histamine, isoproterenol (30 and 120 micrograms/kg), increases[NaCl] in CSF, and nicotine at the higher (1.5 mg/kg) but not lower (0.15 mg/kg) dose. Naloxone increased further (p less than 0.05) the concentration of oxytocin in plasma after histamine, nicotine (0.15 and 1.5 mg/kg), isoproterenol (30 and 120 micrograms/kg) and increases[NaCl] in CSF. Naloxone also increased (p less than 0.05) oxytocin concentration in controls receiving CSF or saline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Naloxone effects on plasma vasopressin and oxytocin concentrations elevated by histamine, nicotine, isoproterenol and an acute increase in [NaCl] in cerebrospinal fluid. 379 91

In urethane-anesthetized rats, injections of 50 pmol of arginine-vasopressin (AVP) or thyrotropin-releasing hormone (TRH) into a lateral cerebral ventricle (i.c.v.) elicit short-latency increases in blood pressure. i.c.v. injection of 50 pmol of the AVP antagonist, d(CH2)5Tyr(Me)AVP, but not of the vehicle (artificial cerebrospinal fluid; a CSF), abolished the pressor action of i.c.v. AVP. The AVP antagonist did not antagonize the TRH-induced pressor responses. In another group of rats, a monopolar stainless-steel electrode was positioned stereotaxically in the paraventricular nucleus (PVN) and pressor responses were elicited by electrical stimulation of the PVN. Micro-injection of 1 nmol of the AVP antagonist, but not of aCSF alone, into the nucleus tractus solitarius/vagal area (NTS/VA), reduced PVN-stimulated pressor responses to 26 +/- 6% of control and stimulation-induced tachycardia to 37.3 +/- 9.0% of control. These studies indicate that the pressor and heart-rate responses to PVN stimulation may be mediated, in part, via AVP receptors in the NTS/VA.
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PMID:Vasopressin antagonist in nucleus tractus solitarius/vagal area reduces pressor and tachycardia responses to paraventricular nucleus stimulation in rats. 392 90

Vasopressin was determined in CSF and plasma of 243 patients with different neurological and psychiatric disorders, including control patients. CSF vasopressin was significantly higher in patients with high pressure hydrocephalus, intracranial tumour, benign intracranial hypertension, intracranial haemorrhage, ischaemic stroke, and craniocerebral trauma. In patients with primary degenerative dementia, CSF vasopressin was lower than in control patients. Among patients with psychiatric disorders, CSF vasopressin was increased in manic patients, while in patients with depression CSF concentration of this hormone did not differ from that found in controls. However, an increase in CSF vasopressin level was found in patients recovering from a depression. The clinical significance of changes in CSF vasopressin concentrations in groups of patients with neurological and psychiatric disorders is still unknown.
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PMID:Cerebrospinal fluid vasopressin in neurological and psychiatric disorders. 397 21

In nine of 102 children admitted to the Montreal Children's Hospital with a diagnosis of aseptic meningitis, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) developed. Patients with and without SIADH were similar with respect to clinical symptoms, duration of illness, and CSF inflammatory response. The SIADH group differed in that the largest age group was 1 to 5 years.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone in enteroviral meningitis. 397 12

During the course of evolution from the beginning of the Caenozoic period, the mammalian species have irradiated into increasingly diverse environments and these physical conditions have imposed powerful selection pressures on the systems of water and salt homeostasis. In the case of physiological actions of hormonal elements of the control systems, effects of antidiuretic hormone and aldosterone on water and salt conservation and of renin-angiotensin II on blood pressure and aldosterone secretion show a general similarity across mammalian species. However, evidence is accruing that there may be large species variation in the vectors of physical, chemical and hormonal changes of the milieu which cause water and salt intake. In the sheep, physiological degree of reduction of CSF [Na] produced by IVT infusion of various hypertonic or isotonic saccharide solutions has a powerful stimulating effect on salt appetite of both Na replete and Na deficient animals. Increasing CSF [Na] reduces appetite. The 0.7 M mannitol CSF infusions initially stimulated thirst but eventually depressed it, presumably due to reduction of CSF [Na]. By contrast, in wild rabbits infusion of 0.9 M mannitol CSF for 2 days at 17 microliter/h caused a large reduction of water intake, a diuresis and no significant increase in salt intake. In laboratory white rats, 0.7 M mannitol CSF infusion at 10 microliter/h for 4 days by Alzet pump, did not increase salt appetite though the infusion was calculated to produce moderate reduction of CSF [Na]. It would appear that there may be significant species differences in effect of reduced CSF [Na] on salt appetite.
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PMID:Species differences in the effect of decreased CSF sodium concentration on salt appetite. 610 Mar 11

Intracerebroventricular (i.c.v.) administration of captopril attenuates the development of hypertension in spontaneously hypertensive rats (SHR). To determine whether these effects are related to inhibition of angiotensin-converting enzyme we assessed the effects of chronic i.c.v. administration of MK-422 (a converting enzyme inhibitor chemically unrelated to captopril) on arterial pressure and vascular reactivity in young (seven-week-old) male SHR. MK-422 (0.2 or 1.0 microgram/h, osmotic mini pump) was infused into the lateral ventrical for 4 weeks. Control SHR received artificial CSF i.c.v., or 0.2 microgram/h MK-422 i.v. Vascular reactivity to phenylephrine, vasopressin and direct sympathetic nerve stimulation was assessed in renal and mesenteric vascular beds using miniaturized pulsed Doppler flow probes. MK-422 attenuated the development of hypertension. Arterial pressure at 4 weeks of treatment was: SHR-i.c.v. MK-422 (0.1 microgram/h): 137 +/- 3.4; (1.0 microgram/h): 138 +/- 2.9; SHR i.v. MK-422 176 +/- 4.5 and SHR control: 168 +/- 4.9 mmHg (P less than 0.01). SHR-i.c.v. MK-422 showed significantly attenuated increases in mesenteric vascular reactivity in response to vasoconstrictors, nerves and sympathetic nervous stimulation. Dose and frequency response curves were characterized by a shift to the right and a significant decrease in the slopes. In conclusion, both captopril and MK-422 prevent the development of hypertension in SHR, presumably by blocking angiotensin-converting enzyme, suggesting that the brain renin-angiotensin system contributes to the pathogenesis of hypertension in that model.
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PMID:Effect of central administration of MK-422 (the diacid form of enalapril) on the development of hypertension in the spontaneously hypertensive rat. 610 Jul 56

A clinical picture compatible with the syndrome of inappropriate ADH (antidiuretic hormone) secretion was observed in two patients receiving vinblastine-bleomycin chemotherapy. The mechanism by which this response is brought about is unclear. Penetration of Vinka alkaloids into CSF of humans is poor in the absence of extensive meningeal involvement, and hence an indirect method of action by a reduction in the osmotic threshold for vasopressin release has been suggested. By administering vinblastine on days 1 and 4 (instead of days 1 and 2, as suggested in the high-response regimen consisting of vinblastine, bleomycin, and cis-platinum) we have found better bone marrow tolerance and have not noticed the inappropriate ADH syndrome.
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PMID:The syndrome of inappropriate ADH secretion secondary to vinblastine-bleomycin therapy. 619 86

The choroid plexus is a major site of CSF production. When primary cultures of bovine choroid plexus epithelial cells were exposed to 1 micrograms/ml cholera toxin, a 50-fold increase of intracellular cyclic AMP was found 1 h later. Exposure of cells to 10(-5) M isoproterenol, 10(-4) M prostaglandin E1, 10(-5) M histamine, and 10(-5) M serotonin caused increases of intracellular cyclic concentrations of 100-, 50-, 20-, and 4-fold, respectively. From 5 to 15 min were required for these maximal responses to occur. Many other molecules including prolactin, vasopressin, and corticotropin did not alter cellular cyclic AMP levels. The accumulation of cyclic AMP could be inhibited by specific antagonists: propranolol inhibited the isoproterenol-mediated stimulation while diphenhydramine and metiamide inhibited the histamine response. In addition, diphenhydramine inhibited serotonin-dependent cyclic AMP accumulation. Combinations of isoproterenol, prostaglandin E1, histamine, and serotonin elicited additive responses as measured by cyclic AMP accumulation with one exception, i.e., serotonin inhibited the histamine response. Our findings suggest that distinct receptor sites on choroid plexus epithelia exist for isoproterenol, prostaglandin E1, and histamine. Efflux of cyclic AMP into the extracellular medium was found to be a function of the intracellular cyclic AMP levels over a wide range of concentrations. Our studies provide direct evidence for hormonal regulation of cyclic AMP metabolism in epithelial cells of the choroid plexus.
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PMID:Hormones and neurotransmitters control cyclic AMP metabolism in choroid plexus epithelial cells. 619 61


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