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)

A relationship was examined between blood vasopressin levels and the fibrinolytic system in 35 patients with angina pectoris (16 with vasospastic angina (VA) and 19 with exercise-induced angina) who had undergone vein occlusion testing. There was a positive correlation between the post-testing vasopressin levels and the activity of tissue plasminogen activator inhibitor (TPAI) (r = 0.54) which was more high in patients with VA (r = 0.61). Only did the patients with VA show a direct relationship between the vasopressin concentrations and the activity of tissue plasminogen activator (TPA) (r = 0.63), the concentration of fibrinogen-fibrin degradation products (FFDP) (r = 0.88). Thirteen patients having higher vasopressin levels (over 3.4 ng/ml) displayed a greater TPAI activity than did the patients with vasopressin levels of at least 3.4 ng/ml (26.2 +/- 4.9 and 15.0 +/- 1.42 IU/ml, respectively; p less than 0.05). There was a direct relationship between the vasopressin levels and the activity of TPA (r = 0.65), the concentration of FFDP (r = 0.78) in patients having a vasopressin level of above 3.4 ng/ml. The findings are in agreement with the concept that endogenous vasopressin is involved in the regulation of the blood fibrinolytic system.
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PMID:[Endogenous vasopressin and fibrinolysis in patients with angina pectoris]. 179 62

Vasopressin and in particular 1-deamino-8-D-arginine vasopressin (DDAVP) can release factor VIII (FVIII) and tissue plasminogen activator (tPA) to the blood. In the present study DDAVP was injected in conscious dogs which had been preloaded with specific antagonists either against vasopressin's vasopressor response (V1-receptors) or its antidiuretic response (V2-receptors). The presence in the blood of either of the antagonists had no effect on the increase of FVIII or tPA following stimulation with DDAVP. It is therefore concluded that the effect of DDAVP on coagulation and fibrinolysis is elicited via a new class of receptors different from the known V1- and V2-receptors.
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PMID:The release of factor VIII and tissue plasminogen activator can not be blocked by specific antagonists to vasopressin. 190 60

We recently showed that the administration of the antidiuretic V2 specific agonist, 1-desamino[8-D-arginine]vasopressin (dDAVP), to seven male patients with congenital nephrogenic diabetes insipidus (CNDI) did not cause a decrease in blood pressure nor an increase in plasma renin activity or factor VIIIc or von Willebrand factor release. In normal subjects, plasma renin activity, coagulation factors and plasma cyclic AMP are stimulated not only by dDAVP but also by the administration of epinephrine. In the present study, we measured tissue plasminogen activator (activity and antigenicity), von Willebrand factor multimers, plasma and urinary cyclic AMP concentrations following dDAVP or epinephrine administration. We infused epinephrine into three male patients with CNDI. Factor VIIIc and tissue plasminogen activator augmented by 75 to 100% and von Willebrand Factor multimers were increased; plasma renin activity and plasma cyclic AMP concentration increased by 200%. None of these values changed when the same subjects as well as eleven other male patients with CNDI received dDAVP. Furthermore, dDAVP administration increased plasma cyclic AMP concentrations in normal subjects, but not in 14 male patients with CNDI. These results demonstrate the specificity of the extrarenal V2 receptor defect expressed in our patients. The lack of a plasma cyclic AMP response to the administration of dDAVP would suggest an altered pre-cyclic AMP stimulation mechanism.
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PMID:Epinephrine and dDAVP administration in patients with congenital nephrogenic diabetes insipidus. Evidence for a pre-cyclic AMP V2 receptor defective mechanism. 255 38

Some patients with von Willebrand's disease do not respond to stimuli such as venous occlusion and infusion of a vasopressin analogue DDAVP. In these patients, fibrinolytic activity is not enhanced and von Willebrand's factor is not released into the blood. Skin biopsies and cryostat sections were used to study the fibrinolytic activity of skin vessels and localization of tissue plasminogen activator (t-PA) in three patients with severe form of von Willebrand's disease. On fibrin films, no fibrinolysis developed around the skin vessels of the patients; however, using specific polyclonal and monoclonal antibodies to t-PA, and peroxidase coupled specific IgG, presence of t-PA antigen was demonstrated in endothelial cells (EC) of all of them. In plasma no t-PA activity was detected either before or after venous occlusion although t-PA inhibitor activity was in a normal range. Small amounts of t-PA antigen was measured in blood by ELISA. From these results, it is concluded that in patients with severe forms of von Willebrand's disease, t-PA present in EC is not functional and can not transform plasminogen into plasmin.
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PMID:Absence of functional activity of tissue plasminogen activator in patients with severe forms of von Willebrand's disease. 311 91

Release of tissue plasminogen activator into the circulation of rats in response to intravascular injections of vasoactive agents is studied by using a sensitive and specific clot lysis assay. Intra-arterial bradykinin elicits a rapid and transient rise in circulating plasminogen activator, which is maximum within one minute and is cleared within four to eight minutes. The plasminogen activator is fibrin dependent and is neutralized by an antiserum to human tissue-type plasminogen activator. Bradykinin is 1,000-fold more potent than the other agonists tested, which include histamine, norepinephrine, epinephrine, eledoisin-related peptide, arginine-vasopressin, lysine-vasopressin, desmopressin acetate, carbachol, and acetylcholine. Potency of bradykinin is related to its amino acid sequence. Sequential infusions of bradykinin produce a tachyphylactoid response that could be overcome by increasing the dose of the sequential bradykinin challenge. It is concluded that the characteristics of the responses to bradykinin and other agents in vivo differ significantly from those observed in isolated tissue preparations.
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PMID:Tissue plasminogen activator release in vivo in response to vasoactive agents. 392 59

Plasminogen can be activated by intrinsic activators that circulate in plasma in a precursor form, by extrinsic activator originating from tissues or the vessel wall and by the exogenous activators, urokinase and streptokinase. Tissue activator and vascular activator are probably identical. Dialysis of plasma against pH 4.0 buffer causes denaturation of the plasmin inhibitors, alpha 2-antiplasmin and C1-inhibitor, while alpha 2-macroglobulin is left intact. Incubation of pH 4.0-pretreated plasma with urokinase or streptokinase at pH 7.5 led to activation of plasminogen and prorenin. Incubation of a plasma fraction, which contained plasminogen and prorenin but no alpha 2-antiplasmin and renin, with highly purified tissue plasminogen activator also led to activation of prorenin. The vasopressin analogue, 1-desamino-8-D-arginine vasopressin (DDAVP), is a potent stimulant for the release of extrinsic activator into the bloodstream. After infusion of DDAVP, 0.4 micrograms/kg, into normal subjects, parallel increments in plasma fibrinolytic activity and renin were observed. Infusion of DDAVP into patients with type IV hyperlipoproteinaemia had little effect on plasma fibrinolytic activity and the response of plasma renin was also subnormal. These observations warrant further studies on a possible role for plasminogen activators in prorenin activation in vivo.
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PMID:Activation of plasma prorenin by plasminogen activators in vitro and increase in plasma renin after stimulation of fibrinolytic activity in vivo. 675 94

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

Although the vasopressin analogue desamino-d-arginine vasopressin (DDAVP) induces a very well characterized increase in factor VIII (FVIII), von Willebrand factor (vWF), tissue plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), the mechanism(s) by which DDAVP enhances the plasma levels of these proteins is poorly understood. Some clinical evidence suggests that certain patients repeatedly treated with DDAVP at closely spaced intervals become progressively unresponsive (tachyphylaxis). In order to investigate the effect of repeated DDAVP infusion on the behaviour of FVIII, vWF, t-PA and u-PA, we infused three different doses of DDAVP (0.3 microgram/Kg) to six healthy volunteers (19-26 years old, mean 22) at 12-hour intervals. Blood samples were collected immediately before and after DDAVP. The second and third infusion of DDAVP induced a low response of FVIII and vWF. In contrast, t-PA and u-PA exhibited a consistent response after each DDAVP infusion. If the progressive decrease of FVIII and vFW response observed in healthy subjects after repeated doses of DDAVP at 12-hour intervals is extended to haemophiliacs and von Willebrand's patients, the usefulness of desmopressin may be limited when these proteins must be raised therapeutically for a prolonged period of time. Finally, our results suggest that the mechanism for regulating the release of vWF and plasminogen activators in the conditions of our study are not dependent.
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PMID:Repeated infusions of DDAVP induce low response of FVIII and vWF but not of plasminogen activators. 832 82

Conflicting results have been reported concerning the effect of the synthetic vasopressin analog desmopressin acetate (DDAVP) on perioperative bleeding and homologous blood requirements in cardiac surgery. Because patients preoperatively treated with platelet-inhibiting drugs are at increased risk of perioperative bleeding, the blood-saving effect of DDAVP was investigated in 40 male patients undergoing primary myocardial revascularization. All patients had taken aspirin within the last 5 days prior to surgery. In a double-blind, randomized trial, the effects of DDAVP (0.3 microgram/kg of body weight) were compared to those of saline placebo on postoperative blood loss and the need to replace blood products. To evaluate the drug's influence on the coagulation and fibrinolytic systems, von Willebrand factor (vWF), the activities of tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI 1), and the split products of cross-linked fibrin (D-dimers) were investigated. The total homologous blood requirement was significantly lower in DDAVP recipients (median 2, range, 0 to 5 U) compared to placebo (median 3.5, range, 0 to 8 U; P < 0.05). Although at all points of measurement (intraoperative and postoperative) transfusion requirement was less in the DDAVP group, hematocrit values of these patients always exceeded those of the placebo group, this difference being significant at the end of the operation. Because no difference in postoperative blood loss was found, the markedly reduced transfusion requirement of the DDAVP-treated patients is explained either by reduced intraoperative bleeding or by a reduced hematocrit of the chest-tube blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of desmopressin acetate on homologous blood requirements in cardiac surgical patients pretreated with aspirin. 840 98

Vasopressin and in particular its structural analogue dDAVP (1-deamino-8-D-arginine vasopressin) can increase plasma concentrations of Factor VIII and tissue plasminogen activator (tPA) in some species of animals and in humans. For this reason dDAVP is used therapeutically in the treatment of bleeding episodes in patients suffering from haemophilia A and Von Willebrand's disease. However, the high antidiuretic activity of dDAVP constitutes and unwanted effect in this context. In the present study, a large number of analogues of vasopressin were designed, synthesized and tested in monkeys with the aim of producing compounds in which the Factor VIII-releasing activity was selectively isolated from the vasopressor and antidiuretic actions of the peptide. The results indicate that it is possible to separate these biological activities; however, none of the analogues tested so far possessed Factor VIII potencies comparable to that of dDAVP.
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PMID:Antidiuretic activity and release of factor VIII by vasopressin analogues. 846 59


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