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

Studies of endothelial regulation of microvascular function have been hampered by the technical difficulty of removing the endothelium without damaging the vascular smooth muscle cells. This study presents a novel method of endothelial damage and lysis based on the facts that endothelial cells express specific antigens and that complement reacts with antibody/antigen complexes, causing cell lysis. We isolated and perfused rabbit glomerular afferent arterioles in vitro and examined vascular responses before and after treating them with an antibody against factor VIII-related antigen and complement. The treatment consisted of perfusing afferent arterioles with medium containing the antibody and complement for 10 minutes, followed by a 20-minute washout period. Before treatment, acetylcholine and the calcium ionophore A23187 (receptor- and nonreceptor-mediated endothelium-dependent vasodilators, respectively) dilated norepinephrine-preconstricted afferent arterioles, whereas neither dilated the arterioles after treatment, suggesting loss of endothelium-dependent vasodilation. In contrast, responses to nicardipine and norepinephrine (endothelium-independent vasodilator and constrictor, respectively) were not altered by the treatment, indicating intact vascular smooth muscle cell function. Transmission electron microscopy revealed that the antibody- and complement-treated arterioles had various degrees of endothelial damage, including areas of detachment from the basement membrane and marked loss of the number and structure of mitochondria, but no evidence of vascular smooth muscle cell damage. These results indicate that treatment with anti-factor VIII-related antigen antibody and complement is an effective method for eliminating endothelium-dependent vasodilation without altering endothelium-independent responses. Thus, this method may be useful for studying the functional role of the endothelium in microvessels.
Hypertension 1994 Jan
PMID:Removal of endothelium-dependent relaxation by antibody and complement in afferent arterioles. 828 76

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.
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PMID:Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. 844 4

Epidemiologic studies have shown a variety of metabolic abnormalities to be risk factors for coronary heart disease. Many of these metabolic risk factors coexist and may have as a common denominator the presence of insulin resistance and hyperinsulinemia. Indeed, clinical studies have demonstrated relationships among blood pressure levels, plasma insulin, fibrinogen, plasminogen activator inhibitor, factor VIII, triglycerides, and total cholesterol levels and other metabolic risk factors. Individuals with hyperinsulinemia generally have low levels of high-density lipoprotein, plasminogen activators, and endothelial relaxing factors as well. New pharmacologic and hygienic treatment strategies that enhance insulin sensitivity and help correct lipoprotein metabolism and other metabolic abnormalities will be critical in maximizing coronary risk reduction in persons with hypertension, diabetes mellitus, or a family history of premature coronary heart disease.
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PMID:Metabolic abnormalities in cardiac ischemia. 856 16

Angiotensin II (Ang II) has growth-stimulatory properties on different renal cell types. However, possible growth effects of this vasoactive peptide on endothelial cells isolated from the glomerular microvasculature have not been formally investigated. Therefore, we isolated and characterized primary cultures of rat glomerular endothelial cells. We used a simple technique in which collagenase-treated glomeruli were sparsely plated in several 96-well culture plates and microscopically screened for cobblestone-like outgrowth. After two limiting dilutions, homogeneous cultures were obtained. Cells were characterized by positive staining for the endothelial markers factor VIII, CD 31, endothelial leukocyte adhesion molecule-1, and the lectin Bandeiraea simplificifolia. Ang II stimulated the synthesis and release of endothelin-1 in culture supernatants. Moreover, in contrast to syngeneic mesangial cells, glomerular endothelial cells expressed angiotensin-converting enzyme. Ang II stimulated a mild but significant proliferation of quiescent cells, as measured by [3H]thymidine incorporation and direct cell counting. This mitogenesis was transduced by losartan-blockade angiotensin type 1 receptors. Moreover, Ang II mediated phosphorylation of mitogen-activated protein kinase 2 and induction of transcripts for the immediate early gene Egr-1. Our results indicate that Ang II is a moderate mitogen for primary cultures of rat glomerular endothelial cells and activation of these metabolically active cells may play a role in the pathophysiology of several types of glomerulonephritis. Moreover, remodeling of glomerular endothelial cells by Ang II may be important in the progression of structural renal damage during the course of hypertensive injury.
Hypertension 1996 Apr
PMID:Angiotensin II is mitogenic for cultured rat glomerular endothelial cells. 861 66

The cross-sectional correlates of three hemostatic factors--fibrinogen, factor VII, and factor VIII--were examined in the Cardiovascular Health Study, a population-based cohort study of 5,201 subjects over age 65 years. Subjects were recruited in 1989-1990 in Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania. In multivariate linear regression models, cardiac risk factors significantly associated with fibrinogen were current smoking, race, lipids, and white blood count. In women, alcohol use, obesity, physical activity, and insulin level were also significant, while in men hypertension was correlated. The significant correlates of factor VII were lipids and white blood count in men and estrogen use, alcohol use, race, lipids, insulin level, white blood count, and obesity in women. The independent correlates of factor VIII were insulin, glucose, and race in both sexes; low density lipoprotein cholesterol, white blood count, and diuretic use in men; and alcohol use in women. In multivariate models, factors known to be modifiable risk factors for cardiovascular disease accounted for more of the population variance of these hemostatic factors in women than in men, especially for factor VII. The hemostatic factors may mediate some effects of risk factors on disease, and this should be considered in longitudinal studies.
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PMID:Association of fibrinogen and coagulation factors VII and VIII with cardiovascular risk factors in the elderly: the Cardiovascular Health Study. Cardiovascular Health Study Investigators. 865 Dec 28

The baseline examination (1987-1989) for the Atherosclerosis Risk in Communities (ARIC) Study was conducted in 15,792 free-living residents aged 45-64 years in four geographically dispersed US communities. A questionnaire on symptoms of transient ischemic attack (TIA) and stroke was evaluated by computer algorithm for 12,205 of these participants. Data were also collected on lipoprotein levels, hemostasis, hematology, anthropometry, blood pressure, medical history, lifestyle, socioeconomic status, and medication use. Noninvasive high resolution B-mode ultrasonographic imaging was used to determine carotid arterial intimal-medial wall thickness (IMT). The cross-sectional relation between the prevalence of TIA/stroke symptoms and putative risk factors was assessed by logistic regression, controlling for age and community. Odds ratios for TIA/stroke symptoms were significantly elevated (p < or = 0.01) for diabetes mellitus, current smoking, hypertension, lower levels of education, income, and work activity, and higher levels of lipoprotein(a), IMT, hemostasis factor VIII, and von Willebrand factor. However, the relations with education and carotid IMT were not present for black Americans. In whites, the relations of TIA/stroke symptoms to IMT were nonlinear. Only at extreme levels of IMT were symptoms substantially more frequent: For example, men with an IMT greater than 1.17 mm or women with an IMT greater than 0.85 mm had approximately twice the odds of having positive TIA/stroke symptoms as those with lower IMTs. The authors plan in future analyses to address the issue prospectively, as well as to examine the relation with magnetic resonance imaging-defined outcomes and clinically defined incident stroke.
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PMID:Association of transient ischemic attack/stroke symptoms assessed by standardized questionnaire and algorithm with cerebrovascular risk factors and carotid artery wall thickness. The ARIC Study, 1987-1989. 889 Jun 64

Elevated platelet activation, fibrinogen deposition in microcirculation, elevation of fibrin/fibrinogen degradation products as well as the increase and decrease in factor VIII concentration are described in pregnancies with hypertension. We analyzed data from 31 pregnancies with chronic hypertension. The aim of this study was to evaluate effects on coagulation factors, pregnancy outcome and fetal growth. An evident change in coagulation factors occurred in pregnancies with hypertension in comparison with healthy pregnant women. Statistically significant coefficient correlation between fetal growth and fibrinolysis were obtained (r = 0.3; p < 0.004). With fibrinolysis slowing down a higher birthweight occurred. Birthweight showed correlation with coagulation factor VIII (r = 0.21; p < 0.03).
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PMID:[Effect of coagulation and fibrinolytic changes on fetal growth in pregnant women with chronic hypertension]. 976 42

The objective of this study was to describe associations of retinal arteriolar abnormalities with clinical and subclinical manifestations of atherosclerosis and a broad group of risk factors for vascular disease. A biracial population of 8772 adults (aged 48 to 72 years) living in 4 communities was examined from 1993 to 1995 were studied for that purpose. Retinal arteriovenous nicking and focal arteriolar narrowing were determined by light-box grading of a 45 degrees fundus photograph by use of a standardized protocol. Diameters of arterioles and venules were measured in digitized photographs, and a summary arteriolar-to-venular ratio was derived as an index of generalized arteriolar narrowing. Focal arteriolar narrowing was associated only with hypertension. Generalized arteriolar narrowing was associated with carotid plaque but not with any other evidence of atherosclerosis, either clinical (cardiovascular disease or stroke) or subclinical (carotid or popliteal artery thickness or lower limb obstructive disease), or with plasma cholesterol. It was also associated with smoking, with inflammatory markers (white blood cell count, fibrinogen, and reduced albumin), and with the triglyceride and high density lipoprotein cholesterol changes associated with inflammation. Arteriovenous nicking was inconsistently associated with subclinical atherosclerosis. It was not associated with cardiovascular disease, stroke, or plasma cholesterol. Arteriovenous nicking was associated with markers of inflammation and vascular endothelial dysfunction (von Willebrand factor and factor VIII). Arteriolar narrowing and nicking appear to be related to hypertension and inflammatory factors. Nicking may also be related to endothelial dysfunction. Results suggest that these arteriolar changes are pathologically distinct from atherosclerosis. Including their measurement in population studies may permit evaluation of the independent contribution of arteriolar disease to various ischemic diseases of the heart, brain, and other organs.
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PMID:Are retinal arteriolar abnormalities related to atherosclerosis?: The Atherosclerosis Risk in Communities Study. 1084 84

Thrombomodulin, an endothelial membrane glycoprotein, is an essential part of the protein C anti-coagulant pathway. It may also have a role in the regulation of fibrinolysis. We carried out a cross-sectional study to assess the association of soluble thrombomodulin (sTM) with peripheral artery disease (PAD) in a stratified random sample (n=863) of otherwise healthy black and white participants of the Atherosclerosis Risk in Communities (ARIC) Study. PAD was more common in black than in white participants and associated with classical risk factors in an expected manner; positively with age, smoking, hypertension, diabetes (P=0.05), and LDL-cholesterol, and inversely with HDL-cholesterol. Significant positive associations were observed also with fibrinogen and white blood cell count. Overall, the sTM concentration was not a significant predictor of PAD. The association was, however, modified by the level of factor VIII:C in whites (P=0.002 for the interaction), but not in blacks. Protein C was inversely associated with PAD prevalence (odds ratio 0.33, 95% CI 0.18--0.61, P=0.0004). sTM was inversely associated with plasminogen, but no associations with t-PA, PAI-1, or D-dimer were seen. In conclusion, the present results provide some additional evidence on the role of thrombomodulin-protein C pathway in atherosclerotic disease and support our earlier observation on interaction between sTM and factor VIII:C.
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PMID:Cross-sectional association of soluble thrombomodulin with mild peripheral artery disease; the ARIC study. Atherosclerosis Risk in Communities. 1147 30

A 47-year old patient who had been suffering from hypertension and chronic renal failure for many years developed progressive extensive haemorrhagic erosions of the mouth within 3 months and less severe erosions of the genital and nasal mucosa. Additionally, subcutaneous haematomas developed spontaneously. Laboratory investigations demonstrated circulating antibodies against factor VIII while direct and indirect immunofluorescent microscopy showed discrete tissue-bound and circulating IgG reactive with the epidermal basement membrane in a pemphigoid-like fashion. Immunoblot analysis of the patient's serum revealed an "atypical" IgG reactivity against a central portion of the extracellular domain of the BP180 antigen. These findings were unexpected, since the clinical aspect showed striking resemblance to (paraneoplastic) pemphigus. The patient developed life-threatening complications. Eventually, reduction of circulating autoantibodies by a combination of plasmapheresis and subsequent immunosuppressive therapy led to a stable remission of both autoimmune bullous skin disorder and acquired haemophilia.
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PMID:[Simultaneous onset of pemphigoid and factor VIII antibody hemophilia]. 1213 99


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