UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes causes the development of atherosclerotic vascular changes. Leukocytes, thrombocytes and also cytokines are involved in this process via endothelial activation. Estimation of interleukin 1 beta (IL-1 beta) and fibrinogen serum level of patients suffering from diabetes in context of endothelial damage is presented. The stage of vascular endothelium damage is based on the measurement of blood endothelial cells (EC) count and concentration of the plasmatic von Willebrand factor (vWF). Endothelial destruction level was established on the base of selectin L, P and E serum concentration. Activation of inflammatory proliferative mechanisms was indicated by IL-1 beta serum level. Serum haemostasis disorders were indicated by fibrinogen concentration. Patients with diabetes t. 1 and t. 2 differentiated by age and diabetes duration time with normal blood pressure and hypertension were included into the research. We showed that in both types of diabetes endothelium damage goes with significant increase of circulated EC count and vWF concentration. Increased serum level of IL-1 beta and fibrinogen in those patients shoulds significant correlation with vascular wall destruction, visibly marked in patients with diabetes t. 2. Hiperfibrinogenaemia and increased IL-1 beta concentration associate with significant engagement of SL and SE in inflammatory proliferative process of endothelium in young people suffering from diabetes t. 1 over 6 years. Hypertension coexisting with essential disease in both types of diabetes remains important progression factor in atheromatic vascular changes.
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PMID:[Contribution of selected factors of inflammatory creative process in the vascular endothelial damage in the diabetes patients]. 1468 2

The most investigated novel risk factors of atherosclerosis are: fibrinogen (Fb), homocysteine (Hcy), lipoprotein (a) (Lp(a)), plasminogen activator inhibitor (PAI-1), markers of inflammation and infectious factors. Atherosclerotic renal artery stenosis (RAS) is a manifestation of generalized atherosclerosis and often coexist with hypertension and renal failure. The aim of the study was to assess plasma concentration of Hcy, von Willebrand factor (VWF), (Lp(a), Fb, PAI-1, and assessment of ACE gene polymorphism in pts with RAS and hypertension. The study included 15 patients with RAS (mean age 51.4 +/- 16.5 yrs) and 27 healthy volunteers (C) (mean age 42.9 +/- 9.5 yrs). Plasma concentrations of Hcy were significantly higher in RAS (11.0 +/- 3.9 mumol/L) than in C (6.8 +/- 1.3 mumol/L). Plasma concentration of VWF was also significantly higher in RAS than C (104.7 +/- 40 vs 73.6 +/- 20%) as was FB concentration (325.9 +/- 70.0 vs 256.2 +/- 54.7 mg%). DD genotype was present in 45% of RAS pts and in 12% of controls. In patients with atherosclerotic RAS novel markers of atherosclerosis may be an additional risk factor in the development and progression of atherosclerotic lesions.
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PMID:[Non-traditional atherosclerosis risk factors in patients with renal artery stenosis and hypertension]. 1497 71

Endothelial microparticles (EMP) are small vesicles released from disturbed endothelial cells (EC). Owing to the central importance of EC injury in thrombotic and inflammatory conditions, assay of EMP as a marker of EC disturbance has come under intensive development by several laboratories. The review begins with established markers of EC injury, commonly soluble markers such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, von Willebrand factor (vWF), etc., pointing out that many of these are in fact mixtures of true soluble molecules with membrane-bound forms, for example, EMP. Assays of EMP from different labs are reviewed and standardization of assay is recommended. EMP are heterogeneous: those released in activation vs. apoptosis are distinctive in phenotypic markers and procoagulant properties. Application of EMP phenotype analysis can distinguish EC state of activation from apoptosis. Some EMP carry functional vWF with properties different from soluble vWF. Certain EMP bind to and activate monocytes; EMP-monocyte conjugates were found to be a marker of inflammatory disease such as multiple sclerosis (MS), and to enhance transendothelial migration of leukocytes in vitro. Clinical studies have revealed elevated plasma levels of EMP in lupus anticoagulant (LA), multiple sclerosis (MS), thrombotic thrombocytopenic purpura (TTP), coronary artery disease (CAD), hypertension, preeclampsia, and diabetes. Further refinement of EMP assay could open new windows for evaluating and monitoring endothelial injury in thrombotic and inflammatory disorders.
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PMID:Endothelial microparticles as markers of endothelial dysfunction. 1497 33

The renin-angiotensin system is the major contributor to development of hypertension, atherosclerosis, and many other cardiovascular diseases. Angiotensin II, one of the main effectors of this system, contributes to the pathogenesis of hypertension and plays an important role in monocyte, platelet, and endothelium interactions. The effects on platelet and endothelial function, either by angiotensin converting enzyme inhibitors or angiotensin receptor antagonists, are still not well understood. A double-blind, randomized, prospective trial of either enalapril (10-20 mg daily) or eprosartan (400-800 mg daily) over a 10-week period was conducted in 42 patients (27 males, 15 females). Platelet activation was evaluated by measuring platelet factor 4 (PF-4), beta-thromboglobulin (beta-TG), the ratio of platelet factor 4 to beta-thromboglobulin, and endothelial function by measuring total plasma nitrate levels, von Willebrand factor (vWF) levels, and blood flow using venous occlusive plethysmography. After a 10-week treatment with enalapril or eprosartan, the sitting blood pressure in both the enalapril group (from 152.2 +/- 18.7 mmHg to 141.9 +/- 23.5 mmHg, P < 0.05) and eprosartan group (from 151 +/- 10.0 mmHg to 142.3 +/- 12.9 mmHg, P < 0.05) was significantly reduced. Significant diastolic blood pressure (DPB) reduction (from 94 +/- 8.7 to 84.5 +/- 9.6 mmHg, P < 0.05) and a greater DBP reduction response were found in the eprosartan group (63% in eprosartan versus 25% in enalapril). Additionally, dose-dependent reductions in the indices of platelet activation and endothelial dysfunction were observed in patients administered high dose treatments of eprosartan and enalapril, and the beneficial effects of these agents were not correlated with the reduction of blood pressure using both agents. Eprosartan is effective and well-tolerated in the treatment of mid-to-moderate hypertension, and the DBP response reduction to eprosartin was better than that to enalapril. A high dose of either eprosartan or enalapril significantly decreased the indices of platelet activation and endothelial dysfunction in hypertensive patients. The benefits of both agents cannot be explained solely by their antihypertensive effects and possibly may be mediated through their unique effect on angiotensin blockade.
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PMID:A double blind randomized trial to compare the effects of eprosartan and enalapril on blood pressure, platelets, and endothelium function in patients with essential hypertension. 1535 73

Although the metabolic syndrome is associated with endothelial damage/dysfunction, the effect of risk factors and their relationship with the development of this condition are unclear. We hypothesized that plasma von Willebrand factor (vWf, marking endothelial damage/dysfunction) increases with the number of components of metabolic syndrome and that increased levels precede its development. To test this, fasting vWf, glucose and lipids were measured in 161 patients (mean age 63 +/- 7 yr, 85% males) with hypertension. Using World Health Organization (WHO) criteria, 32 (19.9%), and using National Cholesterol Education Program (NCEP) criteria, 70 (43.5%) had metabolic syndrome. Plasma vWf was higher in these patients regardless of defining criteria and increased with the number of the components of metabolic syndrome (both P < 0.001). After 4 yr, patients who did not have metabolic syndrome at baseline were reassessed for the development of this condition. Of the 129 patients who did not meet the WHO criteria at baseline, 38 (29.5%) subsequently developed the condition, whereas 36 of the 91 (39.6%) who did not meet the NCEP criteria at baseline subsequently developed metabolic syndrome. Baseline vWf levels did not predict development of metabolic syndrome, regardless of criteria (P = 0.071 for WHO and P = 0.639 for NCEP). Our data suggest more severe endothelial damage/dysfunction with cumulative metabolic syndrome-related risk factors. The failure of plasma vWf to predict the development of metabolic syndrome suggests that endothelial damage/dysfunction is a consequence, not a cause, of these risk factors.
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PMID:Plasma von Willebrand factor and the development of the metabolic syndrome in patients with hypertension. 1553 84

The balance between thrombosis and hemorrhage is carefully regulated. Nitric oxide (NO) is an important mediator of these processes, as it prevents platelet adhesion to the endothelium and inhibits platelet recruitment. Although endothelial NO synthase (eNOS)-deficient mice have decreased vascular reactivity and mild hypertension, enhanced thrombosis in vivo has not been demonstrated. To determine the role of endogenous NO in hemostasis, a model of carotid arterial injury and thrombosis was performed using eNOS-deficient and wild-type mice. Paradoxically, the eNOS-deficient animals had a prolongation of time to occlusion compared with the wild-type mice (P < 0.001). Consistent with this finding, plasma markers suggesting enhanced fibrinolysis [tissue plasminogen activator (t-PA) activity and antigen and D-dimer levels] were significantly elevated in eNOS-deficient animals. Vascular tissue expression of t-PA and platelet activity levels were not altered. In endothelial cells, t-PA is stored in Weibel-Palade bodies, and exocytosis of these storage granules is inhibited by NO. Thus in the absence of NO, release of Weibel-Palade body contents (and t-PA) could be enhanced; this observation is also supported by increased von Willebrand factor levels observed in eNOS-deficient animals. In summary, although eNOS deficiency attenuates vascular reactivity and increases platelet recruitment, it is also associated with enhanced fibrinolysis due to lack of NO-dependent inhibition of Weibel-Palade body release. These processes highlight the complexity of NO-dependent regulation of vascular homeostasis. Such compensatory mechanisms may partially explain the lack of spontaneous thrombosis, minimally elevated baseline blood pressure, and normal life span that are seen in animals deficient in a pivotal regulator of vascular patency.
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PMID:Compensatory mechanisms influence hemostasis in setting of eNOS deficiency. 1556 34

Interest in the endothelium has been growing in recent decades and the traditional belief that it provides an inert interface between blood and the vessel wall is no longer the case. It is now clear that the endothelium produces a large number of substances that influence blood flow, and it is in turn affected by changes in the blood and the pressure of blood flow. Nitric oxide and endothelins are the major regulators of the vascular tone, and thereby the blood pressure. Historically speaking, concepts such as endothelial cell damage and injury were described in the 1960s and 1970s. More recently, terms such as endothelial cell activation and dysfunction have also been introduced. Although similar in some respects or part of a continuum, these terms differ in the actual effects on the endothelium, and hence differentiation is important. In hypertension, the delicate balance between the vasodilators and the vasoconstrictors is upset, with disturbance in the nitric oxide pathways that lead to a predominance of the vasoconstrictors. This in turn leads to many other changes that take place in the endothelium, setting up a vicious cycle that maintains the high blood pressure. Therefore, accurate assessment of vascular function is important in linking pathophysiology with clinical disease, such as hypertension. Indeed, there are several methods currently employed experimentally to assess endothelial dysfunction. However, the most widely studied and accepted tests are the estimation of plasma markers such as von Willebrand factor, E-selectin and thrombomodulin, and studies of forearm circulation in response to hypoxia induced stress ('flow mediated dilatation', FMD) or intra arterially administered drugs such as acetyl choline. The present document examines these topics. Whilst acknowledging the debt owed to animal models in the study of hypertension, we shall focus on work where primary study is in homo sapiens. A greater appreciation of how endothelial assessments are made in hypertension will have relevance for drug development and future management strategies.
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PMID:Endothelial dysfunction: methods of assessment and application to hypertension. 1557 56

As the endothelium is crucial to cardiovascular disease, the accurate assessment of this organ is a valuable tool, especially if such assessments are clinically relevant. As functions of the endothelium focus on haemostasis and the maintenance of correct vascular tone, and dysfunction results in changes that promote thrombosis and hypertension, thus assessment of endothelial function therefore follows these processes. Foremost in the plasma markers of vascular function is von Willebrand factor, a molecule that interacts with platelets. Lack of nitric oxide results in poor blood pressure control that can be quantified by impaired flow mediated dilatation. More recently, increased numbers of circulating endothelial cells have been described that indicate severe damage to the endothelium. Unsurprisingly, these three markers correlate with each other and former two predict adverse outcome in long-term follow up studies. The assessment of vascular damage is becoming recognised as having an increasingly prominent part in the pathophysiology of cardiovascular disease.
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PMID:Assessment of endothelial dysfunction: focus on atherothrombotic disease. 1569 26

In order to maintain an anticoagulant nature, the healthy endothelium secretes factors such as tissue plasminogen activator, ADPase, and expresses membrane thrombomodulin. However, when damaged, it releases increased amounts of pro-coagulants such as von Willebrand factor. Similarly, the healthy endothelium uses nitric oxide, prostacyclin and other molecules to help maintain normal blood pressure, and these molecules also inhibit platelet activity. But a dysfunctional endothelium fails to produce these vasodilators so that vasospasm and hypertension can result. Thus the (damaged/dysfunctional) endothelium can contribute to Virchow's triad by failing to maintain an anticoagulant surface and in failing to correctly regulate blood pressure, factors that are likely to promote thrombosis and hypertension.
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PMID:How a damaged blood vessel wall contibutes to thrombosis and hypertenasion. 1569 58

Endothelial damage, high fibrinogen levels, and platelet activity are the important accelerating factors for the development of hypertension (HT). von Willebrand factor (vWF; endothelial damage marker), fibrinogen levels, and platelet aggregability were compared between patients with uncomplicated, mild-to-moderate hypertension and healthy subjects. The relationship between traditional cardiovascular risk factors and endothelial damage and prothrombotic state was evaluated. One hundred sixty-nine (54 males, 115 females) patients with untreated and uncomplicated mild-to-moderate HT, and age, gender, and body mass index-matched 124 (58 males, 83 females) healthy subjects were enrolled in this study. Plasma vWF, fibrinogen levels, adenosine diphosphate-induced platelet aggregability, insulin, glucose, serum lipids, and uric acid were measured. Patients with HT had significantly increased fibrinogen, vWF, platelet number and aggregability induced by adenosine diphosphate, triglycerides, total/HDL-C, glucose, uric acid levels, and insulin resistance than control group. vWF and hemostatic markers were comparable between smoker and nonsmoker subjects. Platelet aggregability was positively related to systolic and diastolic blood pressure, and vWF. Fibrinogen was positively associated with body mass index (BMI), systolic and diastolic blood pressure, total cholesterol (TC), uric acid, vWF, and insulin resistance. vWF was significantly related to age, systolic blood pressure, TC, LDL-C, and total/HDL-C. Systolic blood pressure was independently related to vWF. vWF and diastolic blood pressure were significant predictors for adenosine diphosphate-induced platelet aggregability. Systolic blood pressure and vWF were independent predictors for fibrinogen levels. Uncomplicated mild-to-moderate HT had endothelial damage and is associated with a prothrombotic state. Traditional cardiovascular risk factors such as age, BMI, dyslipidemia, and insulin resistance are important contributors to the development of endothelial damage and a prothrombotic state. Therefore, it is important to control these cardiovascular risk factors along with proper treatment of HT for preventing target organ damage in mild-to-moderate HT.
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PMID:Endothelial damage and hemostatic markers in patients with uncomplicated mild-to-moderate hypertension and relationship with risk factors. 1582 21

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