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

Preeclampsia or pregnancy-induced hypertension is a major cause of both maternal and fetal-neonatal morbidity and mortality. The deficiency of vitamin E can cause accumulation of lipid peroxidation products, which, in turn, can induce vasoconstriction. This study has examined any evidence of increased cellular lipid peroxidation and accumulation of malonydialdehyde (MDA, an end product of lipid peroxidation) in pregnancy-induced hypertension and any relationship between the elevated MDA and lower vitamin E levels with hypertension in pregnant women. EDTA-Blood was collected from pregnant women at the time of delivery. Plasma vitamin E was determined by HPLC; MDA by the thiobarbituric acid-reactivity. Subjects with diastolic blood pressure (DBP) > or = 90 mm Hg were considered hypertensive (HT) and with < 90 mm Hg normotensive (NT). Data (Mean +/- SE) from 49 NT and 11 HT women show that HT has significantly lower vitamin E (22 +/- 1 vs 27 +/- 1 nmole/ml, p < 0.03) and elevated MDA levels (0.56 +/- 0.06 vs 0.43 +/- 0.02 nmole/ml, p < 0.03) compared to NT; the ages and gestational ages of women were similar. Among all women, there was a significant positive relationship between DBP and MDA levels (r = 0.27, p < 0.05), and a significant negative relationship between vitamin E levels and DBP (-0.36, p < 0.005), and a significant negative relationship between MDA and vitamin E levels (r = 0.27, p < 0.05). Thus, HT women's plasma has significantly lower E and higher MDA levels, and DBP significantly correlates with the extent of vitamin E deficiency and increased MDA levels. This study suggests a relationship between elevated lipid peroxidation and lower vitamin E levels and hypertension in pregnancy (preeclampsia).
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PMID:Relationship between elevated lipid peroxides, vitamin E deficiency and hypertension in preeclampsia. 858 11

Carvedilol is a vasodilating beta-blocker currently marketed for the treatment of mild to moderate hypertension and application is being filed to the FDA for treatment of congestive heart failure. Carvedilol reduces peripheral vascular resistance by blocking arterial alpha 1-adrenoceptors, thereby producing vasodilation, while preventing reflex tachycardia by blocking cardiac beta 1- and beta 2-adrenoceptors. In addition to the safety and efficacy of carvedilol as an antihypertensive agent, experimental studies indicate that carvedilol also provides significant cardioprotection in animal models of acute myocardial infarction as well as protection against the vascular remodelling that occurs following injury of the vasculature. Recent pharmacological studies have uncovered several novel properties of carvedilol which may function to protect the heart and vasculature from chronic pathological processes, such as ischaemia, atherosclerosis and the remodelling that occurs in the heart and blood vessels as a consequence of pressure overload, injury or shear stress. Specifically, carvedilol, likely as a result of the carbazol moiety, is a potent anti-oxidant. In physicochemical, biochemical and cellular assays carvedilol and several of its metabolites inhibit lipid peroxidation, scavenge oxygen free radicals, inhibit the formation of reactive oxygen radicals and prevent the depletion of endogenous antioxidants, such as vitamin E and glutathione. Moreover, carvedilol blocks the oxidation of low-density lipoproteins (LDL), and thereby prevents the formation of oxidized-LDL which is believed to stimulate foam cell formation and augment the development of atherosclerotic plaque. The ability of carvedilol to prevent the formation of oxidized LDL, in addition to the general anti-oxidant properties of the compound, results in the protection of the endothelium from oxygen free radical injury, and thereby prevents the subsequent events triggered by endothelial damage. Recently, carvedilol has also been shown to inhibit vascular smooth muscle cell proliferation and migration. Because carvedilol can inhibit vascular smooth muscle cell proliferation induced by a wide variety of mitogens (e.g. growth factors, angiotensin II, endothelin, thrombin), it is likely that the site of inhibition occurs at some point beyond the specific mitogen receptors, possibly at a distal common pathway that affects the smooth muscle cell cycle. These unique activities of carvedilol have also been confirmed in vivo in a rat model of neointimal formation following vascular injury by balloon angioplasty, where vascular smooth muscle cell migration and proliferation are the key processes involved in the formation of neointima leading to vascular stenosis. In this model, carvedilol suppressed neointimal growth to a remarkable extent ( > 85% inhibition of neointimal formation) at a dose that is similar to the antihypertensive dose used clinically in hypertensive patients. Taken together, these unique multiple actions of carvedilol provide not only for adequate control of elevated blood pressure, but may also provide for protection of the heart and vasculature from secondary damage due to hypertension itself, as well as from other causes, such as ischaemia, pressure overload, shear stress, vascular injury and atherosclerosis.
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PMID:Carvedilol, a novel vasodilating beta-blocker with the potential for cardiovascular organ protection. 873 68

The prevention of coronary artery disease (CHD) and particularly of myocardial infarction (MI) is based on some well designed strategies aimed at treating both asymptomatic high-risk patients (primary prevention) and patients with established CHD (secondary prevention). A positive impact from primary prevention can be basically achieved trough a reduction in high blood pressure and by correcting dyslipidemia. The benefit can be substantially increased by smoking cessation, increasing physical exercise, reduction of body weight, use of post-menopausal oestrogen, moderate alcohol consumption and use of high doses of vitamin E in those patients who are compliant with the specific strategies. Secondary prevention of MI can be again obtained by controlling blood pressure and reducing serum cholesterol in patients surviving acute MI who can also benefit from the administration of beta-blockers, aspirin and probably ace-inhibitors particularly in presence of left ventricular dysfunction. We suggest that in both arms of prevention, significant results can be achieved mainly by a multifactorial approach capable of correcting all the modifiable risk factors that contribute to the rather complex pathogenesis of CHD.
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PMID:Primary and secondary prevention of myocardial infarction. 874 42

Lipid peroxidation is a free radical process which is implicated in the formation of atherosclerosis. Vitamins C and E are important natural antioxidants which inhibit lipid peroxidation and a high intake of these vitamins, particularly vitamin E, is related to a reduced incidence of ischaemic heart disease. Hypertension is an independent risk factor for atherosclerosis and its relationship to antioxidant status is undetermined. In this study, we investigated free radical activity by measuring plasma malondialdehyde (MDA) using high-performance liquid chromatography (HPLC), vitamin C status measured as plasma ascorbic acid and vitamin E status measured as plasma lipid standardized alpha-tocopherol and erythrocyte alpha-tocopherol. We compared 28 patients with essential hypertension to 31 healthy subjects. Results showed that in comparison with the healthy subjects, the hypertensive patients had significantly higher plasma MDA levels (0.95 +/- 0.28 vs 0.69 +/- 0.21 mumol/l, mean +/- SD, p < 0.001) and significantly lower levels of plasma ascorbic acid (34.83 +/- 12.88 vs 51.76 +/- 13.34 mumol/L, p < 0.01). In addition, erythrocyte alpha-tocopherol concentration, which may reflect vitamin E protection in cell membranes, was significantly lower in hypertensive patients when compared with the normotensive controls (3.87 +/- 0.53 vs 4.82 +/- 1.01 mumol/l, p < 0.001), although plasma alpha-tocopherol levels were similar in the two groups (25.07 +/- 10.45 vs 23.96 +/- 6.07 mumol/l). Our results suggest that hypertensive patients may have increased lipid peroxidation and reduced protection from vitamins C and E. This may contribute to the propensity in such patients to develop atherosclerosis.
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PMID:Lipid peroxidation and antioxidant vitamins C and E in hypertensive patients. 882 28

We compared the serum levels of beta-carotene, vitamin A (retinol), and vitamin E (alpha-tocopherol) in healthy pregnant women and their counterparts who exhibited the signs and symptoms of preeclampsia or eclampsia, including: systolic blood pressure greater than 160 mm Hg, edema, and proteinuria. The study was conducted in the cities of Maiduguri and Bauchi, which are located in the semi-arid northeastern region of Nigeria. Most of the pregnant subjects: (1) were teenagers, though they ranged in age from 14 to 25 years; (2) had 2 or fewer prior pregnancies; and (3) were predominantly of the Muslim faith and members of the Hausa, Fulani, or Kanuri ethnic groups. Few of the women had received prenatal care. Serum levels of vitamins A and E and betacarotene were quantified using high pressure liquid chromatography. The serum vitamin A levels of the 9 preeclamptic women (15.3 mg/dL) and the 7 eclamptic women (8.3 mg/dL) were significantly reduced (p < 0.01) relative to the serum vitamin A levels of healthy women in the third trimester (24.2 mg/dL). For the healthy pregnant controls, the levels of vitamins A and E and beta-carotene were relatively constant throughout pregnancy. The mean serum beta-carotene levels for both the preeclamptic and eclamptic groups of subjects were half as high as those of healthy control women in the third trimester (p = 0.004). The serum vitamin E levels of the preeclamptic and eclamptic women were 15% and 30% lower, respectively, than those of the corresponding controls (p < 0.01). The serum levels of these three lipids in the healthy pregnant and non-pregnant women we studied are similar to values reported by others for North American and European women of childbearing age. These results support the hypothesis that preeclampsia-eclampsia deplete natural lipid antioxidants and suggest that the reduced levels of vitamin A in such women experiencing hypertension of pregnancy, if they happen to be infected with the HIV-1 virus, may place them at increased risk for mother-child transmission of the virus.
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PMID:Serum vitamin A, vitamin E, and beta-carotene levels in preeclamptic women in northern nigeria. 886 47

Despite the availability and use of effective methods for limiting infarct size with thrombolytic agents and primary angioplasty, patients experiencing a myocardial infarction (MI) are at increased risk for a second cardiac event in the post-MI period (e.g., reinfarction, heart failure, and sudden death). For this reason, postinfarction risk management is crucial. An extensive data base has firmly established the efficacy of beta blockers in reducing cardiovascular risk following acute MI. The full advantages of angiotensin-converting enzyme (ACE) inhibitors have only recently begun to emerge as the result of a growing understanding of the mechanisms of adverse outcomes following MI. The importance of lipid-lowering agents, in particular the "statins," should be considered in all post-MI patients, especially since recent studies have conclusively shown improved survival and reduced rates of MI and coronary artery bypass surgery in this population with this therapy. Aspirin is now considered a standard part of the early management of the acute infarct patient as well as for secondary prevention in post-MI patients. At present, chronic anticoagulation with warfarin should be reserved for selected patients. The nondihydropyridine calcium antagonists diltiazem and verapamil can be considered for post-MI use only in patients in whom beta blockers are contraindicated and who have preserved systolic function and/or those without clinical heart failure. In contrast, the dihydropyridine calcium antagonists, particularly nifedipine, have no role in secondary prevention. Although long-term benefits are minimal, nitrates continue to be useful in post-MI patients with residual ischemia (angina or silent ischemia), heart failure (systolic or diastolic), or postinfarction hypertension. Antiarrhythmic agents, except amiodarone, are relatively contraindicated in post-MI patients. Recent data show that vitamin E reduces the rate of nonfatal MI. Its role in cardiovascular death and overall mortality remains to be clarified. Despite their demonstrated value, agents used in secondary prevention generally appear to be underutilized. In addition, when pharmacologic therapies are administered for secondary prevention, they are often prescribed at lower doses than those tested and proved in trials. A greater appreciation for the efficacy and safety profiles of these agents could lead to more widespread use and more pronounced reductions in morbidity and mortality among post-MI patients.
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PMID:Pharmacologic therapies after myocardial infarction. 890 Mar 39

Recent studies suggest that vitamin E may be an important preventative factor in the development and progression of atherosclerosis. In order to more clearly define the role of vitamin E in atherosclerosis, we measured vitamin E, conjugated diens, and lipid flurochromes, as well as cholesterol, triglycerides and phospholipid in arterial and venous tissue of 83 patients. Serum cholesterol and triglyceride levels were significantly higher (P < 0.05) in patients with aortic occlusive (AIOD) and aneurysmal (AAA) disease than in control organ donors (OD). Tissue cholesterol concentrations were significantly elevated in AAA tissue when compared to OD and tissue from patients with peripheral occlusive disease (POD). Tissue from patients with AIOD contained greater concentrations of phospholipid (PL) than were measured in patients with POD and in OD. Vitamin E concentrations were highest in POD tissue and approximately 3.0, 2.0, and 1.6 fold greater than OD, AIOD and AAA tissue respectively. Diene conjugates and lipid flurochromes, measures of early and intermediate products of lipid peroxidation, were markedly elevated in all diseased arterial tissue compared to controls. There were no significant differences in tissue or serum lipid levels between saphenous vein (SVBG) and diseased vein grafts (DVG). However, conjugated diene concentrations were elevated in DVG compared to SVBG. Vitamin E levels were significantly elevated in diseased arterial and venous tissue (AIOD, AAA, POD, DVG) removed from patients with diabetes (P = 0.013) and hypertension (P = 0.049) compared to those without these risk factors. Diabetes was the only risk factor associated with significantly increased (P = 0.005) levels of vitamin E when only data from atherosclerotic arterial tissue (AAA, POD, AIOD) were analyzed. These preliminary data provide additional evidence of altered vitamin E metabolism and free radical processes in the tissues of patients with various manifestations of atherosclerosis.
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PMID:Vitamin E levels in human atherosclerotic plaque: the influence of risk factors. 890 54

We evaluated the extent to which cardiovascular risk-reducing behaviors are initiated as a result of knowledge of newly detected coronary artery disease, based on test results from noninvasive electron beam computed tomography (EBCT). A total of 703 men and women, aged 28 to 84 years, asymptomatic and without prior coronary disease, who had a baseline EBCT coronary artery scan and basic medical history and risk factor information completed a follow-up survey questioning them about health behaviors undertaken since their scan. Baseline calcium scores were significantly higher in those who subsequently reported consulting with a physician, or reported new hospitalization, coronary revascularization, beginning aspirin usage, blood pressure medications, cholesterol-lowering therapy, decreasing dietary fat, losing weight, beginning vitamin E, and under more worry (all p <0.01). Other factors, including reducing time worked, obtaining life insurance, losing employment, increased work absenteeism, increasing exercise, or stopping smoking were not associated with coronary calcium. In logistic regression, after adjusting for age, gender, pre-existing high cholesterol, high blood pressure, cigarette smoking, and a positive family history of coronary disease, the natural log of total calcium score remained associated with new aspirin usage, new cholesterol medication, consulting with a physician, losing weight, decreasing dietary fat, new coronary revascularization (all p <0.01), but also new hospitalization (p <0.05) and increased worry (p <0.001). The results suggest that potentially important risk-reducing behaviors may be reinforced by the knowledge of a positive coronary artery scan, independent of preexisting coronary risk factor status.
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PMID:Does coronary artery screening by electron beam computed tomography motivate potentially beneficial lifestyle behaviors? 896 May 87

The study was carried out on 60 oxygen-treated premature infants weighed less than 2000 g (1529 +/- 302 g, x mean +/- S. D.) and on their mothers. Both the Retinopathy of Prematurity screening and the biochemical tests were started at the age of 6 weeks. According to our results, the signs of an acute oxidative stress could be seen in all 60 oxygen-treated prematures erythrocyte's glutathione redox system, independently of the presence of the retinopathy compared to prematures (n = 20) with the same gestational age but without oxygen therapy (1720 +/- 305 g, mean +/- S.D.). The concentrations of free sulfhydril groups in the plasma, and the blood selenium levels were significantly lower in the prematures suffering from moderate retinopathy (n = 5) than in the other oxygen-treated premature without retinopathy (n = 27) and with "any retinopathy" (n = 28) patients groups. The same tendency was seen in the mothers. Vitamin E treatment of "any retinopathy" infants seemed to have a positive effect against the development of Retinopathy of Prematurity. The close correlation found between the antioxidant capacity of the mothers and babies suggest that the supplementation of feeding with sulfur-containing amino acids (methionine, cysteine) during pregnancy would improve the antioxidant capacity of prematures. An antioxidant cocktail (selenium + vitamin E) given to the high-risk mothers (advanced age, smoking, pregnancy-induced hypertension) before delivery as suggested in literature might be useful in prevention of Retinopathy of Prematurity.
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PMID:[Prospective biochemical study of the antioxidant defense capacity in retinopathy of prematurity]. 907 53

Recently, hyperlipidemia as well as hypertension has been observed in Dahl salt-sensitive (S) rats. In this study, to investigate whether the lipid abnormality is involved in the renal injury of Dahl S rats, we examined the effect of vitamin E on glomerular sclerosis, as vitamin E is an inhibitor of lipid oxidation. Dahl S rats were given a high salt diet (8% NaCl) containing either normal vitamin E (2 mg/100 g) or high vitamin E (50 mg/100 g) for 4 weeks. Dahl salt-resistant (R) rats were given a high salt and normal vitamin E diet. The blood pressure in the Dahl rats increased and was not suppressed by the vitamin E supplement. Serum cholesterol and triglycerides in Dahl S rats were higher than in Dahl R rats at both 0 and 4 weeks. Vitamin E lowered the serum cholesterol level in Dahl S rats at 4 weeks (126 +/- 5 v 150 +/- 12 mg/dL, P < .01). Urinary protein excretion and serum creatinine increased in Dahl S rats, and vitamin E inhibited the increases significantly (urinary protein, 70.7 +/- 0.9 v 178.0 +/- 8.8 mg/day, P < .01; serum creatinine, 0.45 +/- 0.02 v 0.63 +/- 0.05 mg/dL, P < .01). Serum lipid peroxide (LPO) was higher in Dahl S rats than in Dahl R rats, and vitamin E lowered LPO in Dahl S rats (2.10 +/- 0.03 v 2.70 +/- 0.04 nmol/mL, P < .01). In the histologic study, sclerosing score (SS) of glomeruli, which represents the degree of glomerulosclerosis semiquantitatively, was higher in Dahl S rats than in Dahl R rats. Vitamin E lowered SS (114 +/- 3 v 157 +/- 6, P < .01) and ameliorated arterial injuries such as medial thickness with partial necrosis and severe fibrinoid proliferation with inflammatory cell infiltration. In all rats, SS was strongly correlated with urinary protein (r = 0.93, P < .01), serum cholesterol (r = 0.86, P < .01), and serum LPO (r = 0.89, P < .01). These results suggest that the renal injury in Dahl S rats is caused not only by hypertension but also by hyperlipidemia. Therefore, vitamin E might ameliorate the renal damage by inhibiting the oxidation of lipids.
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PMID:Vitamin E ameliorates the renal injury of Dahl salt-sensitive rats. 916 Jul 94


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