Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluorescein angiographies of the iris and retina were performed both in normal individuals (104) and in patients suffering from hyperlipoproteinemia (48), maturity-onset diabetes (184), systemic hypertension (12) and atherosclerosis (12). While hyperpermeation of dye located at the pupillary border was seen in 7.7% of the normals, leakages occurred in 66.6% of the hyperlipoproteinemics and in 79% of the recent maturity-onset diabetics. Paraclinical examination of the normal subjects with pathologic dye transit revealed vascular risk factors in each case. Thus, fluorescein iris angiography is a suitable method of detecting vascular damage in cases of metabolic disorder as early as possible.
 ...
PMID:[Value of iris fluorescence angiography in the early diagnosis of vascular lesions]. 406 83

The beneficial effect of antihypertensive pharmacotherapy in decreasing morbidity and mortality in hypertensive patients may be counteracted by metabolic and biochemical disturbances, such as hypokalemia, hyperglycemia, hyperuricemia, and hyperlipoproteinemia, that occur with the administration of thiazides and related diuretics. Antiatherogenic high-density lipoprotein cholesterol may be unchanged, whereas the potentially atherogenic low-density lipoprotein cholesterol may be increased by long-term therapy with thiazide diuretics. Indapamide is a methylindoline antihypertensive diuretic with a considerable peripheral vasodilatory effect. At a low dose of 2.5 mg daily, it did not alter total circulating cholesterol, in contrast to chlorthalidone. High-density lipoprotein cholesterol levels increased significantly in 20 hypertensive men after 6 months of therapy with indapamide, resulting in a significant fall of the low-density lipoprotein/high-density lipoprotein ratio, an atherogenic risk factor, regardless of preexisting lipid disorders.
Hypertension
PMID:Serum lipoprotein levels during long-term treatment of hypertension with indapamide. 407 36

A study was made of the effect of euphylline administration (25 mg/kg) for 20 days on some indicators of carbohydrate, energy, lipid and electrolyte metabolism in blood serum and tissues of the heart, aorta and liver during pituitrin hypertension in rabbits experiencing arterial pressure normalization. It was found that euphylline appreciably decreased hypercholesterolemia and hyperlipoproteinemia seen in hypertension. At the same tine the aortal wall showed a decrease in cholesterol content, in lactate dehydrogenase activity, and the normalization of transketolase activity and calcium concentration. In liver tissue, the activity of glycolytic enzymes was inhibited and cholesterol level declined. The heart muscle manifested a decrease in the activity of glycolytic and pentosephosphate pathway enzymes and in that of creatine kinase. The changes in electrolyte balance included sodium elevation in blood serum, heart and liver tissues.
 ...
PMID:[Effect of euphyllin on metabolic processes in blood and tissues during experimental pituitrin hypertension]. 619 12

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
 ...
PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

Hypertension is a major risk factor for clinically significant atherosclerotic vascular disease in Western Society, although the link between these conditions remains very poorly understood. Recent studies which are reviewed here have demonstrated that major arterial intimal and medial abnormalities occur as a result of hypertension. These include functional changes in endothelial permeability as well as alterations in the endothelial cells themselves with an increase in their turnover and number and distinct changes in morphology. However, endothelial cell loss leading to denudation of the arterial intimal surface appears to be relatively uncommon. Intimal and medial thickening are consistent features of hypertension and result from increases in both cellular and extracellular components. The cells accumulating in the subendothelial space appear to be of both blood-borne and medial origins, although their complete characterization has not been performed as yet. The adherence of blood cells to the endothelial surface appears to be promoted by the presence of hypertension along with their increased entry into the intima through endothelial cell junctions. Medial thickening with hypertension is attributable primarily to increased smooth muscle cell mass, although enhanced deposition of collagen and elastin plays a contributory role. Recent data would indicate that smooth muscle cell hypertrophy rather than hyperplasia is primarily responsible for the greater smooth muscle mass with hypertension. Although elevated DNA content of hypertensive arteries has been demonstrated, such changes may be secondary to a marked increase in cells showing nuclear polyploidy. Prolonged normalization of blood pressure in hypertensive animals can produce considerable regression of arterial changes toward the control state. The changes appear more marked with respect to the cellular rather than the extracellular abnormalities induced by hypertension. In man, little is known about the effects of antihypertensive therapy on the vasculature itself, although clinical complications related to both hemorrhagic or thrombotic strokes are clearly reduced by blood pressure reduction. On the other hand, the influence of treatment on the atherosclerotic process or on the course of coronary artery disease and its complications is not currently understood. The accelerating effect of hypertension on atherosclerosis generally requires a critical level of circulating lipoproteins. Enhanced atherosclerosis is not observed in hypertensive animals without hyperlipoproteinemia or in human subjects with low lipoprotein concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Recent advances in molecular pathology. The effects of hypertension on the arterial wall. 638 Oct 89

A group of 252 chronic hemodialysis patients was examined for various risk factors. Special emphasis was placed upon the comparison of patients who had marked cardiovascular alterations with the remainder of the group. The seriousness of the risk factors was determine by hypertension and hyperlipoproteinemia, 78% of the patients received antihypertensive medication or had changes in the fundus of the eye or both. In 74% of the patients there were pathological changes in the plasma lipids or lipoproteins or both. Hypertriglyceridemia (49%) and a HDL cholesterol decrease (61%) were the most striking findings. The average VLDL cholesterol value was significantly higher and the HDL cholesterol significantly lower in the coronary heart disease group than in the remaining group. These results show that hyperlipoproteinemia and a decrease in HDL, together with other risk factors such as hypertension and anemia, play an important role in the accelerated development of atherosclerosis in a hemodialysis group.
 ...
PMID:Analysis of cardiovascular risk factors in chronic hemodialysis patients with special attention to the hyperlipoproteinemias. 657 64

Interrelation was studied between vitamin C consumption and the prevalence of coronary heart disease and some risk factors in a non-organized male population in Kiev. A reverse relationship was established between vitamin C consumption, the prevalence of coronary heart disease and some risk factors, such as arterial hypertension, hyperlipoproteinemia and overweight.
 ...
PMID:[Relation between vitamin C consumption and risk of ischemic heart disease]. 667 67

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
 ...
PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Using the Princeton School Family Study, our specific aim was to estimate the prevalence of familial hyper- and hypouricemia, to estimate the proportion of probands' first-degree relatives who were similarly affected, and to evaluate the contribution of diseases, drugs, and alcohol intake (if any) to uric acid levels. We studied 379 probands and a total of 1928 subjects, 125 and 52 black probands from a randomly recalled group, 147 white and 55 black probands from a hyperlipidemic recall (top decile cholesterol and/or triglyceride) group. Familial hyper- and hypouricemias were arbitrarily identified in those kindreds having at least two first-degree relatives in the same decile as the proband, top or bottom respectively, for serum uric acid. No probands had symptomatic gout. Diseases, drugs, and alcohol intake were not consistently associated with aggregations of high and/or low uric acid levels in families, and had little relationship to uric acid levels in individuals. Of the 177 randomly recalled probands, and of the 55 black probands in hyperlipidemic recall familial hyperuricemia, with concurrent primary hyperlipoproteinemia and hypertension. Familial hypouricemia was present in 1 of 125 white and in 1 of 52 randomly recalled black kindreds, and in 3 of 147 white and 3 of 55 hyperlipidemic recall black kindreds. While familial clustering of hyperuricemia was limited, clustering of hypouricemia was much more marked. Seventy-four and 84% respectively of first-degree relatives of hypouricemic white and black probands had uric acid less than the 50th percentile. In randomly recalled probands and their first-degree relatives there were significant inverse partial correlations between uric acid and high density lipoprotein cholesterol. Inverse associations of uric acid with high density lipoprotein cholesterol and the concurrence of hyperlipoproteinemia and hypertension in hyperuricemic families points to the importance of lipoprotein and blood pressure screening in families with asymptomatic hyperuricemia. The potential ramifications of within-family clustering of hypouricemia need to be further assessed in populations, particularly in regards to uric acid nephrolithiasis.
 ...
PMID:Familial hyper- and hypouricemias in random and hyperlipidemic recall cohorts: the Princeton School District Family Study. 682 94

Conservative medical treatment is indicated for patients who have stable symptoms of intermittent claudication without rest symptoms or signs, rapidly progressive disease, or disability interfering with gainful employment (see Fig. 1). Valuable general measures include meticulous care of the limbs, avoidance of trauma and infections, and maintenance of normal body weight. Cessation of tobacco smoking is extremely important, and a regimented exercise program is therapeutically beneficial (see Table 1). The high risk factors of diabetes mellitus and hypertension should be controlled. Hyperlipoproteinemia should be treated if present, but it is currently not known if treatment of elevated cholesterol or triglyceride levels prevents progression of or reverses the disease process. If a recent arterial occlusion is suspected, fibrinolytic therapy can be expected to benefit approximately one third of the patients. Anticoagulants and vasodilator drugs have not been shown to be of value. In patients with rest symptoms or signs, who are not candidates for surgical revascularization of the limb, bed rest with dependency of the limb in a warm environment, good foot care, and analgesics are most important. Ulcers should be treated with wet dressings to preserve granulation tissue, and parenteral antibiotics are used if infection is present. When rest symptoms or trophic lesions have disappeared or improved, the patient may be gradually ambulated but should continue to sleep with the head of the bed elevated and should maintain meticulous foot care.
 ...
PMID:Principles of conservative treatment of occlusive arterial disease. 683 16


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>