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

An anthropometric and clinical-instrumental study of 64 males with normolipoproteinemia (NLP) and 106 males with atherogenic hyperlipoproteinemia (HLP) demonstrated, at a rank correlations analysis, that absolute and relative fatty body weight and relative nonfatty body weight correlated, with a high significance, with cardiac output, peripheral vascular resistance and arterial blood pressure, irrespective of NLP or HLP. The hemodynamic profile of males with low, moderate and high fat deposition was associated, respectively, with basic signs of hyper-, eu- and hypokinetic central hemodynamic types. Developing HLP affects central circulatory adaptation to changing fat/nonfatty body weight ratios and may be conducive to arterial hypertension.
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PMID:[The relation of central blood circulation and the values of fatty and non-fatty body weight in men with normo- and hyperlipoproteinemia]. 319 58

Changes in the activity of blood monocytic cholesterol esterase in men with major CHD risk factors (dyslipoproteinemia, arterial hypertension, excessive body mass) were described. Standard methods of epidemiological survey and a radionuclide method to determine cholesterol esterase activity applied to a representative sampling (195 persons) have shown that enzymatic activity was growing with age. In examinees with hyperlipoproteinemia of type IIa and IIb the activity of cholesterol esterase was decreased, and in persons with excessive body mass it was increased. In combination of 2-3 CHD risk factors significant differences in enzymatic activity were undetectable.
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PMID:[Cholesterol esterase activity of blood monocytes and the main risk factors of ischemic heart disease in men aged 20-59]. 321 63

In summary, both the developing atherosclerotic and FSGS lesions seem to share certain postulated pathophysiologic mechanisms, including endothelial cell injury, macrophage infiltration, hyperlipoproteinemia, and hypertension. As depicted in Figure 1, any initial glomerular injury results in flux of macromolecular substances into the glomerular mesangium. As an adjunct to increased glomerular barrier dysfunction, hyperlipoproteinemia is believed to secondarily develop from the dramatic losses of albumin, stimulating increased hepatic lipoprotein synthesis and the loss of lipoprotein lipase-activating substance into the urine which would effectively produce a reduction in circulating chylomicra and triglyceride catabolism. Certain elevated circulating lipoproteins could, theoretically, pass through the damaged glomerular filter into the mesangium, thereby enhancing the flux of macromolecules. Also associated with certain experimental glomerular disorders is the development of glomerular hypertension, as manifested by an elevated glomerular capillary hydrostatic pressure (PGC), which can further augment macromolecular flux into the mesangium. Overloading of the glomerular mesangium by the above mechanisms is believed to be an injurious stimulus for MC to both proliferate and produce excess mesangial matrix substance. Both of these events are thought to be pathologic harbingers of glomerulosclerosis. Glomerular hypertension is also capable of damaging endothelial cells within the glomerular microcirculation, and this purportedly can activate platelets and result in glomerular thrombosis. At present, it is unclear how glomerular thrombosis produces increased mesangial cell injury; however, this process is believed to cause both systemic and glomerular hypertension which may serve as intermediary mechanisms producing the untoward effects of mesangial cell proliferation and matrix overproduction.
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PMID:Focal and segmental glomerulosclerosis: analogies to atherosclerosis. 329 16

Among the risk factors associated with atherosclerotic coronary artery diseases, systemic hypertension and disorders of plasma lipoproteins and apoproteins are very important. Blood lipid changes have been reported with a number of antihypertensive drugs and may conceivably reduce the coronary artery disease-protective benefits of blood pressure reduction. The prevalence of various types of hyperlipoproteinemia among Japanese is discussed, with special reference to the frequency of atherosclerotic vascular diseases. Data concerning the effects of commonly prescribed antihypertensive drugs on blood lipids and apolipoproteins are reported.
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PMID:Effects of antihypertensive drugs on plasma lipids. 366 54

Sustained hypertension (H) was found in 6% of 21,500 school children aged 6 to 15 years studied in 1972-73 and again in 1982-83. The primary character of H was proved in 85%. Hemodynamic studies revealed a hyperkinetic type of circulation and elevated total peripheral resistance. Studies on lipid and carbohydrate metabolism showed a high rate of hyperlipoproteinemia with low levels of HDL-cholesterol and impaired glucose tolerance combined with high basal plasma triglycerides and plasma insulin before and after stimulation by glucose. In a follow-up study 10 years after the first one we established persistent H in 43% of the initially hypertensive children.
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PMID:The Sofia Juvenile Hypertension Study. 375 78

The purpose of this research is to establish in laboratory animals whether a relationship exists among noise exposure, hypertension, and hyperlipoproteinemia. A discussion of the historical background leading to this work is presented. Previous investigations dealing with each of the three variable, noise, hypertension, and hyperlipoproteinemia, as they relate to hearing, are discussed. Methodology, including new methods developed during this study, will be presented. Results support the concept that a significant relationship does exist among noise, hypertension, hyperlipoproteinemia, and hearing loss.
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PMID:Hypertension, hyperlipoproteinemia, chronic noise exposure: is there synergism in cochlear pathology? 376 87

Familial clustering of coronary artery disease (CAD) and familial influences on various clinical and metabolic risk factors were investigated in 85 male survivors of acute myocardial infarction younger than 45 years. The study also involved 85 age-matched men randomly selected from the general population and the first-degree relatives of both patients and control subjects. Presence of CAD was assessed by an angina questionnaire and from rest and exercise electrocardiograms. There was an apparent aggregation of premature CAD in 38% of the case families. A familial clustering of hyperlipoproteinemia was present in 58% of the case families and 15% of the control families. Systemic hypertension and cigarette smoking also were clustered in the case families. Multivariate statistical analyses of clinical and metabolic risk indicators in patients with and without a family history of CAD and in control subjects indicated that familial aggregation of CAD is independently related to MI at a young age. Degree and extent of coronary atheromatosis and number and severity of hemodynamically significant stenoses did not differ between young patients with and without a familial aggregation of CAD. The absence of a relation between the family history and severity of CAD implies that other underlying mechanisms are involved.
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PMID:Risk factors for coronary artery disease in families of young men with myocardial infarction. 381 25

The major atherosclerosis risk factors hypertension, diabetes, hyperlipidemia and cigarette smoking are examined along with blood vessel anatomy, hemodynamics, histopathology and known experimental results. A common factor of blood vessel hypoxia, specifically endothelial and intimal hypoxia, is shown to exist. Arguments are presented suggesting endothelial hypoxia as the commonest initiating event for atherosclerosis. Cholesterol appears to be a secondary and opportunistic villain. Explanations are given for the lack of increased atherosclerosis risk in familial lipoprotein lipase deficiency (type I hyperlipoproteinemia) and for the increased incidence and severity of atherosclerosis in the human abdominal aorta in comparison with the thoracic aorta. It is suggested that effective prevention of atherosclerosis can be accomplished by lowering blood pressure and blood glucose, among others, even though these may be within acceptable normal limits. Suggestions are given for experiments to test the hypothesis of hypoxia being the major initiating factor in atherosclerosis.
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PMID:Mechanisms of atherogenesis: endothelial hypoxia proposed as the major initiator. 385 84

Cardiovascular (CV) risk factors change over time with the emergence of clinically recognizable abnormalities (obesity, hypertension and hyperlipoproteinemia) in the second and third decades of life. A cohort of 286 subjects, aged 11-15 in 1973-74 were reexamined 6 years later to observe changes in height, weight, blood pressure, lipids and lipoproteins between adolescence and adulthood. During the 6 years of follow-up, 10-11 year-old males increased 30 cm in height and 32 kg in weight. Among 10-11 year-old girls, height increased 12-15 cm and weight increased 15 kg in whites and 20 kg in blacks. Mean systolic BP increased 16-23 mmHg in black males and 11-15 mmHg in white males. Mean serum total cholesterol levels increased with age such that levels in 20 year olds were 160-190 mg/dl, about 10 to 15 mg/dl higher than 18 year olds. In white males beta-lipoprotein cholesterol increased (13 mg/dl) with age; however, there was a simultaneous decrease in alpha-lipoprotein cholesterol (11 mg/dl), resulting in a dramatic rise in the beta-LPC/alpha-LPC ratio. These adverse changes in LPC may be related to the early development of atherosclerosis and risk for coronary heart disease of young white men. Early identification of hypertension and hyperlipoproteinemia should help to predict and prevent future CV disease.
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PMID:Transitions of cardiovascular risk from adolescence to young adulthood--the Bogalusa Heart Study: II. Alterations in anthropometric blood pressure and serum lipoprotein variables. 394 31

In numerous studies it has been established that risk profiles of coronary heart disease (CHD) and peripheral vascular disease (PVD) are different. There is no doubt about nicotine++ consumption as the most protective factory of PVD. In order of significance arterial hypertension, hyperlipoproteinemia, diabetes mellitus und reduced physical training are further risk factors. In contrast to CHD, the importance of LDL-cholesterin as arteriosclerotic factor is much lower in PVD while high level of triglyceride is an autonomous risk factor of PVD, as well as physical immobility. In the present review, the different penetrance of risk factors for individual vascular regions are described.
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PMID:[Risk profile in peripheral arterial occlusive disease]. 406 Jul 39


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