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

An oxidant/antioxidant imbalance has been suggested among the pathogenetic factors involved in preeclampsia. As vitamin E is one of the most important antioxidant body components, a nonrandomized controlled trial was undertaken in 36 preeclamptic patients in order to evaluate the effect of vitamin E supplementation (100-300 mg/day per os) on fetal and maternal outcome. Fetal mortality was similar in 14 patients treated with conventional therapy plus oral vitamin E supplementation (35%) and in 22 patients treated with conventional therapy only (36%). Furthermore, in both groups of patients proteinuria increased, and increased dosages of antihypertensive drugs were called for in order to control blood pressure. We conclude that, with these dosages and in case of an already established disease, vitamin E does not improve fetal outcome in severe preeclampsia. Furthermore, it does not show favorable effects on maternal hypertension and proteinuria.
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PMID:Vitamin E supplementation in preeclampsia. 805 Jul 28

Complementary epidemiological studies consistently reveal a substantially increased risk of cardiovascular disease (CVD) at suboptimal plasma levels of essential antioxidants in comparison with optimum ranges of vitamin C (> 50 mumol/l), of lipid-standardized vitamin E (> 30 mumol/l or a tocopherol/cholesterol ratio > 5.2 mumol/mmol), beta-carotene (> 0.4 mumol/l). The poor level of any single essential antioxidant can increase the risk, and the combination of suboptimal levels has additive or even overmultiplicative effects on the risk for CVD. Suboptimal antioxidant levels are stronger predictors of the severalfold regional differences of CVD in Europe than classical risk factor such as hypercholesterolemia, hypertension, etc. Scotsmen and Fins tend to suboptimal levels of essential antioxidants, whereas German-speaking regions may mostly reveal a fair vitamin E status, but at least one out of four subjects can reveal suboptimal levels of vitamin C and carotene, particularly in smokers. This deficit can be avoided by 'prudent diets' rich in fruits and vegetables as practiced by Frenchmen, Italians and Spaniards. The simultaneous correction of all suboptimal antioxidant levels appears to be a promising new means for CVD prevention, particularly in the northern parts of Europe. In the USA the risk of CVD could substantially be reduced without dietary modifications by voluntary daily supplements as follows: vitamin C > 140 mg, vitamin E > 100 IU (100 mg d,l- or 74 mg d-alpha-tocopherylacetate), and in current smokers by gamma-carotene > 8.6 mg. Hence, these antioxidants may be crucial constituents of diets rich in fruits and vegetables, which are by consensus associated with a lower risk of premature death from CVD (and cancer as well).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Essential antioxidants in cardiovascular diseases--lessons for Europe]. 807 84

The effects of age and hypertension on the antioxidant defence systems and the lipid peroxidation in rat isolated hepatocytes were studied. Four different age groups (1, 3, 6 and 12 months) were considered in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Age-associated changes were observed on vitamin E status, glutathione (GSH) level, MDA formation and glutathione peroxidase (GSH-Px) activity in both strains. Maximal levels or activities of these parameters were found at 3 and 6 months, except for MDA which was low at 3 months. Then, a fall was observed at 12-month-old compared to 6-month values. In addition, GSH-Px activity was significantly lower in SHR than in WKY rats, except at the age of one month. The decrease of this enzyme activity could induce an increased cellular generation of radical species and lipid peroxidation, which might be link to hypertension.
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PMID:Age-related changes in antioxidant defence mechanisms and peroxidation in isolated hepatocytes from spontaneously hypertensive and normotensive rats. 807 5

Changes in platelet aggregability patterns and lipid peroxide levels and their relationship were examined in DOCA-salt hypertensive rats during the development of hypertension. In addition, the effect of vitamin E treatment on those changes was also investigated. The blood pressure of the hypertensive rats was 188, 201, 212 mmHg on day 11, 17, and 23, respectively. In the hypertensive rats, both aggregability and granule content in platelet decreased on day 12, 18, 24, and marked decreases were observed on day 24. These data suggested the appearance of exhausted platelets, which had been already activated in vivo due to the hypertension. Marked increases in lipid peroxide levels in serum, the heart and the kidney were observed on day 24 in the hypertensive rats. Increase in serum urea nitrogen was also observed in the hypertensive rats on day 24, suggesting the dysfunction of the kidney. Vitamin E treatment did not prevent in vivo platelet activation due to hypertension, but greatly prevented the elevations of lipid peroxides in serum, the heart and the kidney, and serum urea nitrogen. These results suggested that in vivo platelet activation, an increase of lipid peroxides, and renal dysfunction occur in this order due to hypertension, and that the latter two are significantly prevented by vitamin E treatment.
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PMID:Vitamin E did not prevent platelet activation, but prevented increase of lipid peroxides and renal dysfunction in DOCA-salt hypertensive rats. 812 Jun 68

Oxidation of lipoproteins is hypothesized to promote atherosclerosis and, thus, a high intake of antioxidant nutrients may protect against coronary heart disease. The relation between the intakes of dietary carotene, vitamin C, and vitamin E and the subsequent coronary mortality was studied in a cohort of 5,133 Finnish men and women aged 30-69 years and initially free from heart disease. Food consumption was estimated by the dietary history method covering the total habitual diet during the previous year. Altogether, 244 new fatal coronary heart disease cases occurred during a mean follow-up of 14 years beginning in 1966-1972. An inverse association was observed between dietary vitamin E intake and coronary mortality in both men and women with relative risks of 0.68 (p for trend = 0.01) and 0.35 (p for trend < 0.01), respectively, between the highest and lowest tertiles of the intake. Similar associations were observed for the dietary intake of vitamin C and carotenoids among women and for the intake of important food sources of these micronutrients, i.e., of vegetables and fruits, among both men and women. The associations were not attributable to confounding by major nondietary risk factors of coronary heart disease, i.e., age, smoking, serum cholesterol, hypertension, or relative weight. The results support the hypothesis that antioxidant vitamins protect against coronary heart disease, but it cannot be excluded that foods rich in these micronutrients also contain other constituents that provide the protection.
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PMID:Antioxidant vitamin intake and coronary mortality in a longitudinal population study. 820 76

Possible involvement of reactive oxygen species and nitric oxide in the pathogenesis of human essential hypertension was investigated. It was observed that both superoxide anion and hydrogen peroxide production by polymorphonuclear leukocytes and the plasma levels of lipid peroxides are higher in uncontrolled essential hypertension compared with normal controls. Nitric oxide levels measured as its stable metabolite nitrite, as an index of nitric oxide synthesis, revealed its levels to be low in hypertensive patients. Superoxide anion, hydrogen peroxide, lipid peroxides and nitric oxide levels reverted to normal values after the control of hypertension by drugs. The concentrations of anti-oxidants such as vitamin E and superoxide dismutase were found to be decreased in patients with uncontrolled hypertension. Several anti-hypertensive drugs inhibited lipid peroxidation in vitro. Angiotensin-II, a potent vasoconstrictor, stimulated free radical generation in normal leukocytes which could be blocked by calmodulin antagonists. These results suggest that an increase in free radical generation and a simultaneous decrease in the production of nitric oxide and anti-oxidants such as SOD and vitamin E occurs in essential hypertension. This increase in free radical generation can inactivate prostacyclin and nitric oxide and decrease their half life which can lead to an increase in peripheral vascular resistance and hypertension.
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PMID:Are free radicals involved in the pathobiology of human essential hypertension? 822 35

Seventeen pregnancies with pregnancy-induced hypertension (PIH) and 28 control pregnancies were analyzed with regard to maternal and fetal blood antioxidants and lipid peroxidation products (conjugated dienes). In PIH, maternal blood levels of conjugated dienes were higher than in normal pregnancy. Also the activities of platelet and plasma glutathione peroxidase (GSHPx) were higher in PIH. In umbilical cord blood, the appearance of conjugated dienes, the concentration of vitamin E and the activity of erythrocyte GSHPx were lower than the corresponding maternal values. There was no difference between PIH and normal pregnancy in the appearance of conjugated dienes in cord blood, but erythrocyte GSHPx and plasma vitamin A were lower in PIH. Cord blood plasma vitamin A showed a negative correlation to maternal mean arterial pressure. We suggest that lipid peroxidation is involved in the pathogenesis of maternal PIH, and it may also have effects on the vascular function and antioxidant status of the fetus.
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PMID:Pregnancy-induced hypertension is associated with changes in maternal and umbilical blood antioxidants. 824 88

Abnormal regulation of local vascular tone occurs early in human and experimental atherosclerosis. Impaired endothelium-dependent vascular relaxations mediated by endothelium-derived relaxing factor are an important contributor to these abnormalities. Endothelium-derived relaxing factor is nitric oxide released as such or attached to a carrier molecule. Oxidized lipoproteins impede endothelium-derived relaxing factor-mediated responses in vitro. We designed in vivo experiments to determine whether hypercholesterolemia with and without deficiency of two endogenous lipid antioxidants, vitamin E and selenium, would result in endothelial dysfunction. Vitamin E and selenium deficiencies were induced in a group of hypertension-prone Dahl salt-sensitive rats fed a diet high in cholesterol (4%) but low in NaCl (0.5%) for 18 weeks. Two other groups of Dahl salt-sensitive rats received diets sufficient in vitamin E and selenium but containing either high or normal cholesterol levels (control group). Serum cholesterol levels increased approximately 10-fold in the two groups of rats fed high-cholesterol diets. Systolic blood pressure was 143 +/- 3 mm Hg in high-cholesterol/vitamin E- and selenium-sufficient rats and 142 +/- 5 mm Hg in high-cholesterol/vitamin E- and selenium-deficient rats (P = NS). Mild intimal thickening and occasional mononuclear cell infiltration were observed in both of these groups. Serum vitamin E levels were decreased, whereas serum thiobarbituric acid-reactive substances and exhaled pentane (two indicators of endogenous lipid oxidation) were significantly increased in high-cholesterol/vitamin E- and selenium-deficient rats compared with high-cholesterol/vitamin E- and selenium-sufficient rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1993 Jul
PMID:Hypercholesterolemia promotes endothelial dysfunction in vitamin E- and selenium-deficient rats. 831 92

Ischaemic heart disease remains a major cause of mortality in developed countries. A number of important risk factors for the development of coronary atherosclerosis have been identified including hypertension, hypercholesterolaemia, insulin resistance and smoking. However, these factors can only partly explain variations in the incidence of ischaemic heart disease either between populations or within populations over time. In addition, population interventions based upon these factors have had little impact in the primary prevention of heart disease. Recent evidence suggests that one of the important mechanisms predisposing to the development of atherosclerosis is oxidation of the cholesterol-rich low-density lipoprotein particle. This modification accelerates its uptake into macrophages, thereby leading to the formation of the cholesterol-laden 'foam cell'. In vitro, low-density lipoprotein oxidation can be prevented by naturally occurring anti-oxidants such as vitamin C, vitamin E and beta-carotene. This article explores the evidence that these dietary anti-oxidants may influence the rate of progression of coronary atherosclerosis in vivo and discusses the need for formal clinical trials of anti-oxidant therapy.
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PMID:Can anti-oxidants prevent ischaemic heart disease? 845 85

Carvedilol is a vasodilating, beta-adrenoceptor antagonist currently marketed for the treatment of mild to moderate hypertension. Carvedilol acts to reduce total peripheral resistance by blocking peripheral vascular alpha 1-adrenoceptors, thereby producing systemic arterial vasodilation, while at the same time inhibiting reflex tachycardia through the blockade of myocardial beta-adrenoceptors. In addition to its established efficacy and safety as an antihypertensive agent, carvedilol has been shown to produce significant cardioprotection in experimental animal models of acute myocardial infarction, with the most dramatic effect being observed in the pig model of myocardial ischaemia and reperfusion, where the reduction in infarct size reached 91%. Recent pharmacological studies have revealed additional novel properties of carvedilol which may account for the marked protection produced by the drug in the ischaemic myocardium and which may also result in protection against other chronic pathological processes, such as atherosclerosis and acute vascular injuries. The latter arise from surgical procedures, such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting. Specifically, carvedilol, as well as some of its hydroxylated metabolites, are potent antioxidants. In physicochemical, biochemical and cellular assays, carvedilol and several of its metabolites prevent lipid peroxidation and the depletion of endogenous antioxidants, such as vitamin E and glutathione. Moreover, carvedilol and its metabolites prevent the oxidation of LDL to oxidized LDL, the latter being directly cytotoxic and known to activate monocytes/macrophages and to stimulate foam cell formation. In addition, carvedilol was found to inhibit both rat and human vascular smooth muscle cell proliferation and migration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carvedilol, a novel multiple action antihypertensive agent with antioxidant activity and the potential for myocardial and vascular protection. 852 83


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