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)

Non-enzyme fibrinolytic agents include pharmacological agents which are active in vivo but inactive in vitro and synthetic chemical compounds which when added to blood or plasma in vitro directly induce fibrinolysis. There are a number of drugs with a short duration of action such as adrenalin, nicotinic acid, vasopressin and histamine. Vasoactive drugs probably act by stimulating the liberation of vascular activator. The effect of nicotinic acid is rapidly exhausted when injections are repeated. By contrast, the biguanides and certain anabolic steroids are capable of exerting a long term stimulation of endogenous fibrinolysis. Amongst these substances, phenformin, metformin, ethyloestrenol, stanozolol and a new substance, moroxydine chloride, have been studied. The biguanides appear to be capable of exerting an effect upon the synthesis and liberation of plasminogen vascular activator. The combination of an anabolic steroid and a biguanide would appear to be the most powerful. These various drugs have been used with success in cases of recurrent venous thrombosis in patients with an abnormally low level of plasminogen activator in the venous walls and/or low fibrinolytic activity after venous stasis. Chemical fibrinolytic agents were studied only in vitro, since the use of these substances in human therapeutics would seem to be still difficult in view of the fact that they are active only in a narrow range of concentrations.
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PMID:[Non-enzymatic fibrinolytic agents]. 3 Nov 13

Structural requirements of the systemic factor VIII response to intravenous vasopressin in man has been investigated using vasopressin analogues. With the analogues available the receptor specificity of this phenomenon could not be distinguished from those associated with the previously described plasminogen activator release or antidiuretic effects of this hormone. Further studies using 1-desamino-[8-D-arginine]vasopressin showed a dose-related release of both procoagulant and antigenic components of the factor VIII complex. The newly released factor VIII could not be distinguished from circulating factor VIII on the basis of molecular size, electrophoretic mobility or in vitro stability despite apparent differences in the duration of response of the procoagulant and antigenic components in vivo.
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PMID:Specificity in the factor VIII response to vasopressin infusion in man. 42 46

In eight patients with cirrhosis of the liver and portal hypertension an intravenous infusion of lysine vasopressin induced a rapid increase in the plasma level of the fibrinolytic proenzyme plasminogen activator. In contrast, triglycyl lysine vasopressin (glypressin; GVP), in a dose known to lower portal venous pressure, produced no fibrinolytic response. This lack of fibrinolytic response represents an advantage of GVP over lysine vasopressin in addition to its longer in vivo half-life and lower cardiotoxicity. Clinical trials of GVP in the treatment of bleeding oesophageal varices are needed.
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PMID:Effects of lysine vasopressin and glypressin on the fibrinolytic system in cirrhosis. 48 51

The influence of substances known as low molecular weight mediators such as biogenic amines, peptides and prostaglandins on the plasminogen activator release was studied in the isolated perfused pig ear. Among the substances tested, histamine and the plasma kinins bradykinin and kallidin were found to possess a dose-dependent activator-releasing effect, which in case of histamine can be suppressed by an antihistamine (promethazine). Serotonin and the prostaglandins at concentrations up to 10(-5)M possess no significant activator-releasing effect. Compared with the biogenic peptides angiotensin, oxytocin, vasopressin, and eledoisin, only the latter was found to release plasminogen activator. Studies on the influence of the substances tested on the capillary permeability showed that enhanced permeability is caused only by those mediators which cause also increased activator release.
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PMID:[Influence of mediators on plasminogen activator release]. 75 12

Adrenaline, nicotinic acid (NA), vasopressin (LVP) and other drugs affecting vascular motility are known to increase plasminogen activator (PA) and factor-VIII plasma levels in man. To evaluate the hypothesis that NA, LVP and adrenaline release PA from the endothelial cells of the vessel wall through their common effect on vascular motility, PA has been characterized by means of a histochemical technique on vein biopsies obtained from human volunteers after infusion of the compounds. Furthermore, the effect of single and repeated administration has been compared in order to investigate whether the pattern of PA and factor-VIII variations in plasma is similar with the three drugs. There was no major difference in the PA content of the veins following the marked and sustained increase of the corresponding plasma activities. A simple explanation is that the intensity and duration of the stimulus may not be sufficient to deplete the large stores of the vessel walls. The magnitude, time course and duration of the plasmatic response after single and repeated infusions was on the whole different and peculiar for each drug. A derivative of LVP which is free of vasoactive actions was more effective than LVP in inducing the responses, which could also be elicited in two anephric subjects. These findings suggest that vasoactivity is unlikely to provide the clue to a common pathway for the fibrinolysis and coagulation response after the compounds, and support the existence of different specific receptors.
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PMID:Mechanism of plasminogen activator and factor VIII increase after vasoactive drugs. 119 76

To produce anti-idiotypic antibodies against receptors for the neurohypophyseal hormone vasopressin, an anti-vasopressin monoclonal antibody with a ligand specificity similar to that of vasopressin receptors was employed for immunization. Three anti-idiotypic monoclonal antibodies were obtained which induced, like vasopressin, plasminogen activator production in the renal epithelial cell line LLC-PK1 (expressing V2-receptors). Induction of plasminogen activator synthesis by the anti-idiotypic antibodies could be inhibited by coincubation with a vasopressin antagonist. In a fashion similar to that of vasopressin itself, the anti-idiotypic antibodies induced receptor down-regulation. The anti-idiotypic antibodies were employed to visualize vasopressin receptors on LLC-PK1 and A7r5 (V1-receptor-expressing) smooth muscle cells by immunofluorescence. Antibody-mediated fluorescence was not observed in receptor-deficient mutant cell lines or vasopressin-receptor-down-regulated cells. Furthermore, these antibodies were used for immunohistochemical localization of vasopressin receptors in rat and bovine kidney preparations. In accordance with earlier physiological and biochemical observations, vasopressin receptors were detected predominantly in collecting ducts in cortex and medulla. On the cellular level, a differential staining pattern was observed.
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PMID:Generation of anti-idiotypic monoclonal antibodies recognizing vasopressin receptors in cultured cells and kidney sections. 142 42

1. During major abdominal surgery there are increases in Factor VIII and plasminogen activator activity, associated with elevated plasma concentrations of vasopressin, of a magnitude shown to affect haemostasis. 2. To investigate the mechanisms involved in the haemostatic response to surgery, 12 patients undergoing fibre-optic colonoscopy were studied, of which six had a complete and six had an incomplete examination. 3. Venous blood samples were taken before, during and after the procedure for assay of plasma vasopressin, adrenaline and noradrenaline concentrations, Factor VIII coagulant activity, von Willebrand factor antigen level, euglobulin clot lysis time, tissue-type plasminogen activator activity and tissue-type plasminogen activator inhibition. 4. In the six patients who underwent a complete procedure the median plasma vasopressin concentration rose from 0.6 pg/ml to 153 pg/ml during colonoscopy. Factor VII coagulant activity rose from 0.9 to 2.4 i.u./ml and von Willebrand factor antigen level rose from 139 to 224%. Plasminogen activator activity increased from 20 to 144 units and tissue-type plasminogen activator activity rose from 107 to 1338 m-i.u./ml, whereas tissue-type plasminogen activator inhibition fell from 4.8 to 1.0 i.u./ml. 5. In the six patients in whom a limited procedure was performed, there were no changes in haemostatic function or in plasma vasopressin concentration. Plasma concentrations of adrenaline and noradrenaline did not change in either group. 6. The results indicate that vasopressin regulates the intrinsic coagulation pathway and fibrinolytic system in the absence of adrenaline release.
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PMID:Haemostatic responses and vasopressin release during colonoscopy in man. 165 70

Fibrinolytic responses to infusion of 1-desamino-8-D-arginine-vasopressin (DDAVP) were assessed in 6 males with congenital nephrogenic diabetes insipidus (NDI), 6 carriers of the NDI gene and 6 normal control subjects. Tissue-type plasminogen activator (t-PA) activity and antigen increased significantly in normal subjects, while plasminogen activator inhibitor (PAI) activity decreased. None of these changes were observed in patients with NDI. In 2 female carriers, normal fibrinolytic responses were seen, while in the other carriers responses were delayed. These findings are consistent with the concept of a general V2-receptor defect in congenital NDI. DDAVP tests are of limited use in NDI carrier detection.
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PMID:Fibrinolytic responses to 1-desamino-8-D-arginine-vasopressin in patients with congenital nephrogenic diabetes insipidus. 189 7

Plasma concentrations of plasminogen activator activity (PAA) and factor VIII are partly controlled by circulating adrenaline and vasopressin. Acute rises in PAA and factor VIII occur during electroconvulsive therapy (ECT). To investigate the relationships between vasopressin (aVP), adrenaline and changes in PAA and factor VIII during ECT, 8 female and 2 male patients, median age 57 years (range 39-75) undergoing modified ECT had venous blood samples taken before and at 2 min, 15 min, 60 min and 24 h after cessation of seizure activity. AVP rose from 0.5 before ECT to 35.5 pg/ml at 2 min (P less than 0.005) and fell thereafter. PAA (10(6)/ECLT2) increased from 22 to 69 units (P less than 0.005) over the same time and fell to 13 units at 24 h (P less than 0.02). Tissue plasminogen activator activity (tPA) rose from 162 before to 1447 mIU/ml at 2 min. (P less than 0.005) and its inhibition activity fell from 8 to 3.75 IU/ml (P less than 0.005) over the same time and rose to 10.4 IU/ml after 24 h (P less than 0.02). There were no changes in adrenaline, noradrenaline, factor VIIIc, vWF or fibrinopeptides A and B beta 15-42. AVP correlated with tPA (rs = 0.64, P = 0.0022) and PAA (rs = 0.61, P = 0.004). These results support the hypothesis that aVP has a role in the regulation of fibrinolytic activity mediated by an increase in tPA. The absence of a factor VIII response may indicate that adrenaline is more important in the regulation of factor VIIIc and vWF.
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PMID:The effect of modified electroconvulsive therapy on vasopressin release and haemostasis in man. 212 14

Three patients with congenital, nephrogenic diabetes insipidus (NDI) from two unrelated families were tested for haemostatic and fibrinolytic responses to DDAVP infusion and venous occlusion. None of the three patients showed a response of factor VIII:C, vWF:Ag or t-PA to DDAVP, a V2-agonist. However, the baseline levels of these factors in the patients' plasma were normal and during venous occlusion a rise in t-PA antigen and t-PA activity was observed in all patients. One patient showed a definite response of the t-PA antigen level to exercise. It is concluded that (extrarenal) V2-receptor-mediated responses are absent in these patients, but that baseline homeostasis and the response to venous occlusion and physical exertion are intact. Presumably, these depend on other mechanisms. This observation denies a central role for vasopressin receptors in the on-demand regulation of clotting and clot dissolving properties of the blood.
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PMID:Normal homeostasis of fibrinolysis in nephrogenic diabetes insipidus in spite of defective V2- receptor-mediated responses of tissue plasminogen activator release. 213 55


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