Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipoprotein(a) (Lp(a)) has been established as an important independent risk factor for the development of cardiovascular disease. Apolipoprotein(a), together with apo B-100 the apolipoprotein of Lp(a), is homologeous to plasminogen but lacks fibrinolytic capacity and appeared to interfere with fibrinolysis in in vitro and ex vivo experiments. We determined the correlations between Lp(a) and other blood lipids (serum cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), coagulation parameters (fibrinogen, factor VII, factor VIII:C fibrin monomers, thrombin-antithrombin III) and fibrinolysis parameters (tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and D-dimer) in 54 patients with essential hypertension, in 65 non-insulin-dependent diabetic patients and in 116 insulin-regulated diabetic patients. Signs of activated coagulation and increased reactive fibrinolysis were found in all three patient groups. In the hypertensive patients, Lp(a) was significantly correlated with LDL-cholesterol (r = 0.25, P = 0.04) and triglycerides (r = -0.30, P = 0.03), while in insulin-regulated diabetics, Lp(a) was also correlated with LDL-cholesterol (r = 0.20, P = 0.03). In the hypertensive patients and both diabetic groups there was no correlation of Lp(a) with coagulation or fibrinolysis parameters. These data show that Lp(a) concentrations are not related to coagulation or fibrinolysis parameters in hypertensive or diabetic patients and confirm the presence of an activated coagulation system in these patient groups.
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PMID:Low order correlations of lipoprotein(a) with other blood lipids and with coagulation and fibrinolysis parameters in hypertensive and diabetic patients. 138 33

Plasma protein C and serine protease inhibitors together with some other hemostasis parameters have been determined in 60 patients with essential hypertension. Significant decrease in protein C and alpha 2-antiplasmin levels, increased fibrinogen, fibrinopeptide A, WF: Ag, plasminogen, and prolongation of euglobulin fibrinolysis time have been observed. Results indicate hypercoagulability and fibrinolysis defect in hypertensive patients.
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PMID:[Protein C and plasma serine protease inhibitors in patients with essential hypertension]. 166 85

Fibrinogen, fibrinogen-related antigen (FR-antigen), and components of the fibrinolytic enzyme system were measured in patients with essential hypertension, renal disease with and without hypertension, and normal subjects. Essential hypertension was associated with a decrease in plasminogen activator and an increase in FR-antigen. In renal disease these changes were accompanied by increases in plasminogen activation inhibitor, alpha(2)-macroglobulin, alpha(1)-antitrypsin, and fibrinogen.
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PMID:The fibrinolytic enzyme system in hypertension. 471 59

A highly-standardized plate method was used to study fibrinolytic profiles in 14 patients with essential hypertension and 245 normotensive healthy control subjects. Compared with the normotensive group, the group with essential hypertension showed a defect in fibrinolysis, as evidenced by a significant increase in the mean level of inhibitor of plasminogen activation, and a subset of the hypertensive patients also showed a significant decrease in the mean level of vascular plasminogen activator. There were no significant differences between the two groups in relation to plasma fibrinogen level, total fibrinolytic activity and plasmin inhibitor. The alterations in inhibitor of plasminogen activation and vascular plasminogen activator in the patients with essential hypertension may reflect a defect in the fibrin-clearing mechanism and, perhaps, contribute to the vascular complications of hypertension.
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PMID:Abnormalities of fibrinolysis in essential hypertension. 624 55

The contact phase of blood coagulation in a group of patients suffering from essential hypertension was studied before and after captopril administration. The baseline levels of factor XII, factor XI and plasminogen were significantly higher than in normals and correlated with baseline diastolic blood pressure levels. On the contrary, plasma prekallikrein was not significantly different from normal. These results suggest the presence of a hypercoagulable state in essential hypertension. After captopril administration, factor XII, factor XI and prekallikrein rapidly decreased, perhaps as a consequence of the drug's effect on the vascular endothelial surface. There was no correlation between the changes of active and inactive renin and the changes of prekallikrein and plasminogen levels. Our data do not support the view that factor XII-plasma kallikrein or plasmin dependent pathways are involved in the activation of inactive renin in vivo. Captopril, by provoking rapid pressure changes, appears to be able to affect the clotting system.
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PMID:The contact phase of blood coagulation and renin activation in essential hypertension before and after captopril. 638 34

The incidence of atherosclerotic and thromboembolic complications is quite high in hypertensive patients. Blood platelets and fibrinolytic activity may play an important role in the development of these complications. We investigated fibrinolytic activity and in vivo platelet release reaction in essential hypertension. Plasma levels of beta thromboglobulin (BTG), platelet factor-4 (PF4), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1) and plasminogen were determined in 36 essential hypertensive and 20 age and sex-matched control subjects. Plasma BTG levels were significantly higher in the hypertensive subjects than in controls (p < 0.05), whereas PF4 levels were similar for both groups suggesting an increase of in vivo platelet activity. PAI-1 antigen levels were found to be significantly higher in the hypertensive patients as compared to the control subjects (p < 0.01). On the other hand significant variations of t-PA antigen and plasminogen values were not observed in the two groups. These results suggest that essential hypertension is associated with decreased fibrinolytic activity and enhanced platelet activity as evidenced by high plasma levels of PAI-1 and BTG.
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PMID:Fibrinolytic activity and platelet release reaction in essential hypertension. 789 22

The fibrinolytic activity was measured in 30 patients with essential hypertension and 15 patients with acute cerebral infarction. The content of plasminogen (PLG) and plasminogen activator inhibitor-1(PAI-1) were higher in the patients with essential hypertension than in the controls. The results suggested that the fibrinolytic activity had a potential tendency towards decreasing in the patients with essential hypertension. The fibrinolytic activity was lower in the stage of cerebral attack and was higher in the stationary stage of acute cerebral infarction, which showed that a change of the fibrinolytic activity in acute cerebral infarction was related to the clinical course.
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PMID:[Changes in the fibrinolytic activity in hypertension and acute cerebral infarction]. 824 28

Endothelial damage, platelet hyperactivity and other changes of blood coagulation may play a role in the vascular complications of essential hypertension. Undesirable changes of haemostasis induced by some anti-hypertensive drugs can encourage the acceleration of atherogenesis. Therefore, the effect of angiotensin-converting enzyme (ACE)-inhibitors on haemostasis is of interest. The therapeutic dose of perindopril was previously shown to reduce platelet aggregation. In the present study, selected parameters of haemostasis were investigated in 23 patients with first and second stage of non-treated essential hypertension. The measurements were carried out before therapy, after 1 week of placebo administration, and after 1 week and after 1 month of ACE-inhibitor perindopril therapy in a once-daily dose of 4 mg. Plasma prothrombin time, activated partial thromboplastin time, fibrinogen level, plasminogen and antithrombin III activities, protein C and free protein S antigens, total fibrinolytic activity as well as fibrin monomers and D-dimers were assayed. There were no significant changes in any haemostasis variables investigated following placebo administration or perindopril therapy. On the basis of this study, no unfavourable effects on haemostasis induced by this therapy were found. The platelet-inhibitory effect of perindopril, without any harmful effects on coagulation or fibrinolytic activity and coagulation inhibitors, is desirable in the new approach to hypertension treatment. These properties of perindopril may be important in terms of the beneficial role of anti-hypertensive drugs in cardiovascular morbidity.
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PMID:Effect of the angiotensin-converting enzyme inhibitor perindopril on haemostasis in essential hypertension. 1108 84

High plasma plasminogen-activator inhibitor-1 (PAI-1) concentrations have been reported in coronary artery disease and stroke. We therefore, prospectively studied the association of PAI-1 with early target organ damage in patients with arterial hypertension has not been clearly established. We therefore investigated 136 subjects, 64 males and 72 females, mean age 50.0 +/- 12.3 years, with newly diagnosed essential hypertension who were free of cardiovascular events and were not receiving any antihypertensive medication. Plasma PAI-1 levels were measured by an ELISA method (STAGO). The study population was divided into two groups, group A with PAI-1 levels below 40 ng/mL and group B with more than 40 ng/mL. The left ventricular mass was calculated according to the formula of Devereux and was normalized by the individual's body surface area (LVM/BSA). Carotid intima-media thickness (IMT) was determined by ultrasonography. Microalbuminuria was assessed by an immunoturbidimetric method (SERA-PAK). Group A consisted of 89 individuals with hypertension (65.4%), 41 males and 48 females and group B of 47 individuals with hypertension (34.6%), 21 males and 26 females. Individuals in group B exhibited significantly higher LVM/BSA than individuals in group A (155.9 +/- 23.1 g/m2 vs. 129.7 +/- 32.2g/m2, respectively, p = 0.004) and increased IMT (0.97 +/- 0.20mm vs. 0.87 +/- 0.21 mm, respectively, p < 0.001). Microalbumin excretion rate was greater in group B than group A (70.9 +/- 84.4 mg/24 hrs vs. 20.9 +/- 45.1 mg/24 hrs, respectively, p = 0.002). In conclusion, elevated PAI-1 levels are associated with target organ damage in subjects with newly diagnosed arterial hypertension. Thus, it can be postulated that this fibrinolytic inhibitor may characterize hypertensives in the early stages of the atherothrombotic process.
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PMID:Increased plasma plasminogen activator inhibitor-1 levels: a possible marker of hypertensive target organ damage. 1259 20

Etiopathogenesis of arterial hypertension and coronary disease involves interaction of numerous exogenous factors which determine the clinical course and therapeutic response in genetically predisposed individuals. The role of numerous cardiovascular risk factors has been reevaluated during the past few years, yet some unresolved issues and gaps still remain. One of the still insufficiently studied factors is lipoprotein (a) [Lp (a)] which belongs to a subclass of LDL lipoproteins. Its important component is apolipoprotein (a) which is structurally similar to plasminogen. This characteristic can be followed through evolution and is probably crucial for its physiologic but also pathophysiologic role. Actually, through its competition with plasminogen, Lp (a) interferes with the process of fibrinolysis and may contribute to tissue healing and restoration but also support and accelerate atherothrombotic process. Lp (a) concentration is stable and genetically determined in an individual and the indication that persons with elevated levels are permanently exposed to increased risk is supported by the data on twofold incidence of myocardial infarction in mothers of children with highest Lp (a) concentrations. Apart from competing with plasminogen via apolipoprotein (a), Lp (a) increases the activity of inhibitors of plasminogen-I activator and reduces the activity of transforming growth factor-beta. This results both in the absence of fibrinolysis and promotion of migration and proliferation of media smooth muscle cells, which are important in the onset of atherosclerotic process. Lp (a) binds to elastin via apolipoprotein B, resulting in oxidation and facilitated entry into macrophages and their transition into the so-called foam cells, also an important sign of early atherosclerosis. Although many pathophysiologic processes by which Lp (a) contributes to atherosclerosis have also been confirmed by animal experiments as well as by the presence of histologic evidence, clinical significance of elevated Lp (a) concentration is still questionable. However, results of prospective studies and metaanalyses were published few months ago and identified decisively Lp (a) as a factor that increases cardiovascular risk primarily in patients in whom other risk factors were also present. According to currently prevailing attitude, routine determination of Lp (a) is not justified and, according to most authors, its determination is useful in patients who had a cardiovascular incident at the age under 55 years, in those with recurrent coronary stenosis, or those with positive family history of such incidents. As Lp (a) is genetically determined, its detection in the early stages of essential hypertension might be a useful prognostic marker but a period of observation is still necessary for correct selection of hypertensive patients. Apart from the observation that hormone replacement therapy significantly decreases the Lp (a) level, there is currently no information on the effectiveness of either dietary or drug therapy. Due to Lp (a) antifibrotic effects, small aspirin doses may be beneficial to these patients, as well as B complex vitamins since hyperhomocysteinemia enhances atherogenicity of Lp (a). Therapeutic approach to patient with increased Lp (a) levels is currently based on as strict regulation of arterial pressure, glycemia and other dislipidemias as possible. In the present clinical practice, the elevated level of this lipoprotein indicates a patients with elevated cardiovascular risk, regardless of the fact whether Lp (a) is only a marker or an active factor of pathophysiologic process. Increased Lp (a) concentration may refer to the need for therapy, frequent monitoring and determination of even stricter aims for these individuals by selecting metabolically neutral and best tolerated drugs.
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PMID:[Lipoprotein (a)--a mysterious factor in atherogenesis]. 1267 78


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