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 renal concentrating ability was studied in 11 subjects by means of 14-16 hours of fluid deprivations, alone and in combination with the vasopressin analogue desmopressin. The effect of desmopressin without fluid deprivation on urinary osmolality was also studied. The combination of desmopressin and fluid deprivation was not superior to fluid deprivation alone for the production of concentrated urine. Desmopressin alone was inferior to the other two methods. No difference in renal concentrating ability could be demonstrated after 14 hours of fluid deprivation, when comparing 118 subjects exposed to various organic solvents with 48 controls.
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PMID:Studies on kidney function in subjects exposed to organic solvents. II. The effect of desmopressin in a concentration test and the effect of exposure to organic solvents on renal concentrating ability. 725 66

Desmopressin (1-desamino-8-D-arginine vasopressin (DDAVP)) is a synthetic analog of arginine vasopressin (AVP) and is useful in the treatment of some bleeding disorders. The mechanism of improved hemostasis in patients with platelet dysfunction is uncertain. Platelet-rich plasma samples from 35 normal subjects were incubated with serial dilutions of DDAVP, AVP, and adenosine diphosphate. The expression of the platelet activation-dependent antigen CD62 (P-selectin) was measured by fluorescent-labeled monoclonal antibody and flow cytometry. DDAVP at concentrations of 1.0 to 1000 nmol/L stimulated significant expression of CD62 on normal platelets in vitro. At a pharmacologic concentration of DDAVP (1 nmol/L), 14.1% (0.6% to 45.4%) (median and range) of platelets expressed CD62. There was a strong correlation between DDAVP-induced and AVP-induced CD62 expression (rs = 0.62, p = 0.0008) but not between DDAVP-induced and ADP-induced expression, suggesting a V1 receptor-mediated mechanism. Preincubation of platelets with a vasopressin V1 receptor antagonist completely inhibited CD62 expression in response to DDAVP. We conclude that DDAVP directly activates platelets by interaction with the platelet V1 receptor in vitro. This finding may partially explain in vivo effects of DDAVP on hemostasis.
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PMID:Desmopressin stimulates the expression of P-selectin on human platelets in vitro. 756 50

Desmopressin (DDAVP), an analog of vasopressin (AVP), has wide clinical application as an anti-hemorrhagic (AH) agent. DDAVP in vivo releases vWF from endothelial cells but is reported to have little action on platelets. However, DDAVP is often used to improve hemostasis in platelet dysfunctions. We examined the effect of DDAVP on platelet microparticle (PMP) formation and procoagulant activity in vitro using platelets from normal volunteers and in vivo in six patients receiving DDAVP therapy. In the former, platelets were incubated with DDAVP (0.5 to 25 nM) and PMP released were stained with FITC-labeled MAb alpha-GP IIb/IIIa for flow cytometry. Procoagulant activity was measured in a clot-based assay using Russel's viper venom (RVV) calibrated with cephalin. A mean increase of 2-3 fold was observed in both PMP and procoagulant activity. Parallel to these observations was a dose-dependent rise in organelle-associated Ca2+. The assays were also performed on six patients prior to and at one hour after infusion of DDAVP, and similar but lesser effects were observed. We conclude that DDAVP acts on platelets in vitro, and that these effects may contribute to the hemostatic action of DDAVP in platelet dysfunctions in vivo.
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PMID:Desmopressin (DDAVP) acts on platelets to generate platelet microparticles and enhanced procoagulant activity. 767 3

Dextran 70 and the haemostatically active vasopressin analogue desmopressin were administered to four healthy volunteers and to 12 patients undergoing total hip replacement. In volunteers the antidiuretic effect of a single i.v. dose of desmopressin (0.3 microgram/kg bodyweight) caused a mean net urine deficit, compared with controls, of 890 ml/24 h. Both drugs increased estimated blood volume, but only the combination caused an increase still persisting after 24 h (+530 ml). Desmopressin-treated surgical patients had the same urine volumes as controls, without the use of more diuretics or more i.v. fluid administration. Creatinine clearance was significantly increased postoperatively in patients on desmopressin, compared with controls. Thus the long-lasting antidiuretic effect of desmopressin seen in healthy volunteers was absent in surgical patients, possibly because there was a compensatory increase in glomerular filtration rate (creatinine clearance).
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PMID:Renal effects of high dose desmopressin and dextran. A study in normal subjects and in patients undergoing total hip replacement. 767 11

Desmopressin is a widely used hemostatic drug. It is a synthetic analogue of the natural hormone vasopressin, but, in contrast to vasopressin, it has no pressor activity. The effect is immediate, with two- to sixfold increases in the plasma concentrations of coagulation factor VIII, on Willebrand factor, and tissue plasminogen activator, and increases in platelet adhesiveness of comparable magnitude. Desmopressin is used in patients with mild hemophilia A, von Willebrand's disease, congenital platelet dysfunction, or acquired platelet dysfunction due to uremia or intake of such drugs as aspirin. It may also be used to reduce surgical blood loss in patients without known bleeding diathesis. Optimal hemostatic effect is achieved with a dosage of 0.3 micrograms/kg given intravenously. Other routes of administration are subcutaneous injection or intranasal spray. The latter proved to be efficient for home treatment of patients with bleeding disorders.
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PMID:Desmopressin (DDAVP) and hemostasis. 794 3

Intravenous (i.v.) infusion of the selective vasopressin (V2) agonist 1-desamino-8-D-arginine vasopressin (DDAVP, Desmopressin) in humans causes a fall in blood pressure, an increase in heart rate, and a rise in plasma renin and noradrenaline. The present study was designed to demonstrate the vasodilatory properties of DDAVP in the renal circulation and to describe the effect of DDAVP on renin secretion. Seven male subjects (31-63 years) with hypertension, who showed no signs of renal parenchymal disease, received an i.v. infusion of DDAVP (400 ng/kg in 10 minutes). They were studied at the time they were undergoing renal vein renin sampling and renal angiography as part of the diagnostic work-up of their hypertension. 131I-Hippurate clearance was used to measure effective renal plasma flow (ERPF). True renal plasma flow was calculated as ERPF divided by the renal extraction ratio of 131I-hippurate. 125I-Thalamate clearance was used to measure glomerular filtration rate (GFR). Measurements were made before and 15-20 minutes after administration of DDAVP. Angiography was performed in the same session after the last blood samples had been collected. In all patients the renal arteries were normal and the extraction ratios of 131I-hippurate and 125I-thalamate (Ehip, Ethal) were not different for the left and right kidney, and in all seven patients a diagnosis of essential hypertension was made. After DDAVP systolic blood pressure decreased by 14.4 mmHg (2.0-26.8) (mean, 95% confidence interval, p < 0.05). Diastolic blood pressure decreased by 12.1 mmHg (2.9-21.7, p < 0.01). Heart rate increased by 17.5 bpm (11.7-23.2, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of DDAVP on renal hemodynamics and renin secretion in subjects with essential hypertension. 795 85

Desmopressin and vasopressin were injected into the blood supply of the bilaterally perfused nasal mucosa of the dog. Nasal vascular resistance and, in some experiments, nasal airflow resistance and the secretory output of the lateral nasal gland were measured on both sides. Systemic arterial blood pressure was recorded. Desmopressin caused a dose-related vasodilation on the side of injection with no changes in systemic arterial blood pressure or secretion by the lateral nasal gland. Nasal airflow resistance did not change significantly. Vasopressin increased nasal vascular resistance on the side of injection with no changes in the systemic arterial blood pressure or secretion by the lateral nasal gland. Nasal airflow resistance did not change significantly. Thus desmopressin dilates the nasal vascular bed and vasopressin constricts it. The relevance of these findings to the use of the two agents applied into the nose in clinical practice is discussed.
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PMID:Actions of desmopressin and vasopressin on the perfused nasal vasculature of the dog. 802 81

Desmopressin is a potent antidiuretic for nocturnal enuresis with few and mostly insignificant adverse reactions. Almost 80 years ago, the antidiuretic effects of extracts of the posterior pituitary were first reported. The molecular structure of the peptide vasopressin arginine vasopressin (AVP) became known in 1956, and by 1967, a synthesized modification of AVP, known as DDAVP, or desmopressin, was introduced. Toxicity studies performed on experimental animals support the conclusion that desmopressin is considerably more potent as an antidiuretic than AVP and has an exceptional safety margin. Further, clinical experience reveals that from 1974 to June 1992 only 21 patients using desmopressin had serious adverse reactions (water intoxication), and no fatalities occurred. Seven of 10 children with nocturnal enuresis who receive desmopressin stop their bedwetting completely or reduce it significantly, with best results noted in children over 10 years of age. Given these results, the preferred treatment in Europe for children with nocturnal enuresis is the sequential combination of desmopressin and the enuresis alarm.
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PMID:Efficacy, safety, and dosing of desmopressin for nocturnal enuresis in Europe. 803 34

Conclusive evidence of a polyuric etiology from a failure of vasopressin elevation led to a new pharmacologic approach to the treatment of childhood nocturnal enuresis. Desmopressin acetate, a vasopressin analogue, has been used successfully since 1978 to treat this condition. Desmopressin's efficacy at doses of 5 to 40 micrograms has been demonstrated in Europe and the United States. Similarly, its safety has been established, and it is a first-line choice for physicians worldwide.
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PMID:The American experience with desmopressin. 803 36

The effects of diazepam on rat renal function were investigated by means of clearance techniques in conscious animals. Different intravenous doses of diazepam were tested: 0.1, 0.3 and 10 mg/Kg body weight A marked increase in fractional water, sodium and potassium excretion was found in every group studied. This alteration was associated with a urine-to-plasma osmolality ratio diminution. On the other hand, no modifications in glomerular filtration rate or p-aminohippuric acid clearance were observed. The reabsorption of water in collecting tubule in diazepam treated rats was decreased as compared with control rats. To assess diazepam-effects on collecting tubule response to vasopressin, the effects of desmopressin on concentrating ability in control and diazepam-treated rats were tested. Desmopressin-treatment promoted a significantly lower free water reabsorption in diazepam-treated group as referred to control rats. This results indicate that diazepam may promote impairments on renal tubular ions reabsorption and that it modifies the collecting tubule response to desmopressin.
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PMID:Evidence that diazepam elicits alterations on rat renal function. 821 Jun 91


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