Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A change in the response of the blood coagulation system to the intravenous injection of vasopressin (AVP), DDAVP and DGAVP has been studied in the experiments on white rats. Intensification of the procoagulant activity on AVP is of the dose-dependent character. Maximal effect is observed 5-15 min after i.v. injection of AVP in a dose of 4 mg/kg. The administration of this peptide increases the fibrinolytic activity, that is connected with an increase in the level of plasminogen activator. DDAVP and DGAVP have a weaker effect on fibrinolysis. AVP and DDAVP increase the level of FVIII by 5-6% during the first minutes, but DGAVP increases the level of FVIII only after 15-30 minutes. While using AVP, DDAVP and DGAVP in clinical practice it is necessary to allow for their hormonal action, the initial state of haemostasis and the age of patients.
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PMID:[Effect of vasopressin and its analogs on blood coagulation in rats]. 239 44

The prolonged partial thromboplastin time observed in the plasma of a 36 year old asymptomatic man was related to the reduced prekallikrein activities (coagulant; antigenic; and amidolytic) and the absence of coagulant and immunologic activities of high molecular weight kininogen (HMWKg). The patient's plasma also exhibited impaired surface-mediated fibrinolysis and impaired generation of kallikrein. The coagulation defect was identified as the "Fitzgerald trait". The levels of CH50, C2, C4 and C-1 inactivator were normal. Venous occlusion in the patient gave rise to a normal release of extrinsic plasminogen activator from the vascular endothelium. The administration of DDAVP led to a FVIII/VWF response which was similar to that obtained in healthy subjects. No alteration could be observed in the contact phase proteins after DDAVP administration.
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PMID:New congenital deficiency of high molecular weight kininogen and prekallikrein (Fitzgerald trait). Study of response to DDAVP and venous occlusion. 363 67

We studied a Spanish family in which one of the female members presented recurrent thrombophlebitis in both legs after three different deliveries. Biological and antigenic activity of protein C was decreased (35% and 42% respectively). Reduced protein C levels were also observed in 6 other family members. Administration of danazol (600 mg/day) in two patients with protein C deficiency elevated this protein and discontinuation of the drug resulted in a reduction of protein C to pretreatment values. The proposita showed a normal fibrinolytic activity and infusion of DDAVP produced a similar response of FVIII/VWF and plasminogen activator to those observed in healthy subjects.
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PMID:Protein C deficiency--response to danazol and DDAVP. 384 Feb 87

Plasma concentrations of vasopressin (aVP) attained under conditions of stress were simulated by infusing four volunteers with 0.25, 0.5, 1.0 and 2.0 pressor units of aVP over 1 h (units/h). Three subjects had all four infusions and one received only 1.0 unit/h. Blood samples were taken for assay of factor VIII coagulant activity (FVIIIC), factor VIII related antigen (FVIIIRAg), the ristocetin cofactor (FVIIIRiCof), euglobulin lysis time (ELT) and aVP concentrations before infusion (time 0) and every 20 min for 80 min. Fibrinopeptide A (FPA) generation time was measured at time 0, 60 and 80 min. At infusion rates of 0.25 unit/h median aVP levels peaked at 6.5 pg/ml and there was no change in FVIII or FPA generation time, and plasminogen activator activity (10(6)/ELT2) rose from 100 to 400 units. At 1.0 unit/h, aVP levels rose to 25.4 pg/ml, FVIIIC rose by 160% and activator activity from 87 to 360 units. At 2.0 units/h, aVP concentrations reached 83 pg/ml, there was an increase in all modalities of FVIII and activator activity rose from 251 to 452 units. FPA generation time shortened and circulating plasma levels of FPA were increased. There was a highly significant correlation between the percentage increases in all three components of FVIII and plasma aVP levels (FVIIIC: r = 0.87, P less than 0.0001; FVIIIRAg: r = 0.61, P less than 0.0001; FVIIIRiCof: r = 0.80, P less than 0.0001) and between the increase in plasminogen activator activity and aVP levels (r = 0.56, P less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of physiological concentrations of vasopressin on haemostatic function in man. 393 Jan 28

In healthy subjects, intravenous infusion of the selective V2-vasopressin receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP, 400 ng/kg in 10 min) causes a marked increase in heart rate with a slight decrease in diastolic blood pressure. These haemodynamic responses are associated with increments in the plasma levels of renin, noradrenaline (NA), clotting factor VIII (FVIII:C), von Willebrand factor (vWF:ag), and tissue-type plasminogen activator (t-PA), and a fall in the plasma level of plasminogen activator inhibitor (PAI). None of these changes was observed in 3 patients with congenital nephrogenic diabetes insipidus (NDI), who had a genetic defect of the V2-receptor. Plasma AVP levels in these patients were normal or slightly elevated, which makes it unlikely that the lack of DDAVP responsiveness was caused by down-regulation of vasopressin V1-receptors. In one NDI patient, arginine vasopressin (AVP) was given in incremental doses (62.5-4000 pg/kg/min). The heart rate and blood pressure responses to AVP were normal, indicating the absence of a V1-receptor defect. The responses of vWF:ag and t-PA to venous occlusion in the patients with NDI were similar to those in 5 healthy volunteers, which indicates that in NDI the endothelial release of both vWF:ag and t-PA is normal. We conclude that DDAVP causes its effects on heart rate and blood pressure, and on the plasma levels of renin, noradrenaline, FVIII:C, vWF:ag, and t-PA through V2-receptor stimulation.
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PMID:1-Desamino-8-D-arginine vasopressin (DDAVP) in patients with congenital nephrogenic diabetes insipidus. 823 94

We studied exercise-induced changes in coagulation and fibrinolytic factors and activation products in different age categories. Thirty-eight sedentary males, divided in three age categories (cats I-III; 20-30, 35-45 and 50-60 y) were subjected to a standardized exercise test. Pre-exercise levels (cats I-III resp) of FVII:c (105 +/- 5, 121 +/- 6 and 123 +/- 7% NP), fibrinogen (2.35 +/- 0.12, 2.55 +/- 0.10 and 2.66 +/- 0.09 mg/ml), prothrombin activation fragment F1 + 2 (0.80 +/- 0.10, 0.80 +/- 0.11 and 1.22 +/- 0.16 nM), t-PA (5.2 +/- 0.6, 9.2 +/- 1.0, 8.6 +/- 1.2 ng/ml) and PAI-I (42.8 +/- 7.5, 67.6 +/- 7.6, 62.2 +/- 10.9 ng/ml) showed differences that seemed related to age. Regression analysis revealed associations with anthropometry (FVII:c, fibrinogen, F1+2, t-PA, PAI-1) rather than with age. Exercise-induced changes in coagulation (increase in von Willebrand factor and FVIII:c and a shortening of APTT) and fibrinolytic potential (increase in t-PA and u-PA) were of comparable magnitude for the three age categories. Hardly any change in F1 + 2 (6%) was observed, while thrombin-antithrombin complexes (93%), plasmin-antiplasmin complexes (79%) and D-dimer (77%) almost doubled during maximal exercise. We conclude that anthropometric differences play a more significant role than age on constitutive levels of haemostatic factors in participants up to 60 years of age. The magnitude of exercise-induced changes is comparable in the age categories under study, and simply super-imposed on constitutive (pre-exercise) levels. Clear evidence for prothrombin activation is lacking, but plasmin formation is enhanced during exercise.
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PMID:Changes in haemostatic factors and activation products after exercise in healthy subjects with different ages. 877 20

Twenty-five young subjects were divided into experimental (n = 13) and control (n = 12) groups in order to examine the acute and chronic effects of exercise on blood coagulation and fibrinolysis. Blood coagulation and fibrinolysis variables were ascertained in both groups before and after a physical conditioning programme both at rest and following maximal exercise. The experimental group exercised for 12 weeks [30 min, 3 x week at 70% (6 weeks) and 80% (6 weeks) of maximum heart rate]. The control group maintained normal activity patterns. Significant activation (P < 0.05) of blood coagulation was observed in response to maximal exercise before and after the conditioning programme in both groups in activated partial thromboplastin time (APTT), thrombin clotting time (TCT), factor VIII procoagulant activity (FVIII PA) and factor VIII antigen (FVIII A). Likewise, blood plasminogen activator showed a significant increase (P < 0.05) in response to maximal exercise before and after conditioning in both groups. Although VO2 max following the conditioning programme was significantly increased in the exercise group versus control, no significant changes (P > 0.05) were observed in either group in blood coagulation and fibrinolysis parameters at rest or in response to maximal exercise. It is concluded that maximal exercise transiently accelerates blood coagulation and activates blood fibrinolytic activity, however physical conditioning appears not to influence the haemostatic and fibrinolytic systems at rest or in response to maximal exercise.
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PMID:Blood coagulation and fibrinolysis at rest and in response to maximal exercise before and after a physical conditioning programme. 882 26

Desmopressin (DDAVP) 0.3 micrograms/kg was infused in 20 uremic patients with prolong bleeding time. Prior to infusion, the uremic patients had a reduced level of tissue plasminogen activator (t-PA), normal levels of von Willebrand factor antigen (vWF:Ag) and ristocetin cofactor activity (vWF:RCo) and elevated level of factor VIII coagulant activity (FVIII:C). Patients with lower hematocrit or t-PA levels tended to have a longer bleeding time. One hour after DDAVP infusion, the bleeding time was shortened significantly. This improvement was significant in all patient groups irrespective of the high or low initial levels of factor VIII complex components. Plasma levels of FVIII:C, vWF:Ag, vWF:RCo and t-PA all increased significantly. The magnitude of increase in these factors, however, was not significantly correlated with the extent of bleeding time shortening. The multiple regression model for predicting the extent of bleeding time shortening suggested only two variables, viz initial bleeding time and posttreatment FVIII:C activity to be of significance. The present results indicate that the hemostatic response to DDAVP is uniform in uremic patients, regardless of whether the initial activities of factor VIII complex components are high or low. Posttreatment FVIII:C activity appears to play a significant role in the hemostatic action of DDAVP. Furthermore, a depressed fibrinolytic activity was generally observed to concur with the hemostatic defect in uremic patients.
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PMID:Hemostatic and fibrinolytic response to desmopressin in uremic patients. 908 15

Involvement of AVP in several pathological states is now established and specific modulation of the different AVP receptor subtypes (V1a, V1b and V2) offers new clinical perspectives for treating major diseases. Recent years have marked a turning point with the design and the use of the first nonpeptide vasopressin receptor antagonists expressing various selectively profile. In that field, we report here the characterization of SR 121463A a highly selective, orally-active antagonist of vasopressin V2 receptors in several models in vitro and in vivo. This compound displayed competitive nanomolar affinity for V2 receptors in various species including man and exhibited a highly selective AVP V2 profile. In vitro, SR 121463A potently antagonized AVP-stimulated adenylyl cyclase activity in human kidney preparations (Ki = 0.26 +/- 0.04 nM) without any intrinsic agonistic effect. In normally-hydrated rats, SR 121463A induced dose-dependent powerful and long-lasting aquaresis after intravenous (0.003 to 0.3 mg/kg) or oral (0.03 to 10 mg/kg) administration. The action of SR 121463A is purely aquaretic with no changes in urine Na+ and K+ excretions unlike that of known diuretic agents such as furosemide or hydrochlorothiazide. In vasopressin-deficient Brattleboro rats, SR 121463A is devoid of any V2 antidiuretic agonist properties. In addition, this compound potently antagonized DDAVP extrarenal V2 effects on hemostasis factor release (FVIII, vW and t-PA) in dogs (ID50 approximately 10 micrograms/kg i.v.). Thus, SR 121463A is the most potent and selective, orally-active V2 antagonist yet described. It is a useful ligand for exploring V2 receptors and the therapeutical usefulness of pure V2 aquaretic agents in several water-retaining diseases and congestive heart failure.
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PMID:Nonpeptide antagonists for vasopressin receptors. Pharmacology of SR 121463A, a new potent and highly selective V2 receptor antagonist. 1002 34

The influence of age on training-induced changes in resting and stimulated hemostatic potential was studied in three age categories (Cat I-III; 20-30 yr, 35-45 yr, and 50-60 yr, respectively) of sedentary men before and after 12 wk of training. Coagulation, fibrinolytic activity, and activation markers (reflecting fibrin formation and degradation) were determined. Physical conditioning resulted in a more pronounced increase in von Willebrand factor (vWF) and factor VIII clotting activity (FVIII:c) in Cat I and II and a more pronounced shortening of the activated partial thromboplastin time in all categories at maximal exertion and during recovery. Enhanced increases in tissue-type plasminogen activator (t-PA) antigen and activity and single-chain (sc) urokinase-type plasminogen activator (u-PA) at maximal exercise and 5 min of recovery were observed in all age groups after training. The effects on FVIII:c, vWF, and scu-PA were most pronounced in the youngest age group (Cat I). Increases in the marker of thrombin generation were highest in Cat III; no effect was seen on thrombin-antithrombin complex, plasmin-antiplasmin complex, and D-dimer in any of the age groups. We concluded that training enhances both coagulation and fibrinolytic potential during strenuous exercise. The effect on FVIII/vWF and t-PA/u-PA is most pronounced in younger individuals, whereas thrombin formation is most pronounced in older individuals.
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PMID:Aging, physical conditioning, and exercise-induced changes in hemostatic factors and reaction products. 1079 12


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