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

Epidemiological studies suggest that intrauterine undernutrition plays an important role in the development of arterial hypertension in adulthood. Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have antioxidant properties that could improve redox-sensitive vascular changes associated with hypertension. The authors determined whether vitamins C and E treatments ameliorate the hypertension and vascular function in male rats submitted to intrauterine undernutrition. Pregnant Wistar rats were fed either normal or 50% of the normal intake diets during the whole gestational period. At 14 weeks of age, male offspring of nutritionally restricted dams were divided into 3 subgroups: vehicle-treated (vehicle for 15 days, by gastric gavage, n = 9), vitamin C-treated (ascorbic acid, 150 mg/Kg/d for 15 days, by gastric gavage, n = 15) and vitamin E-treated (alpha-tocopherol, 350 mg/kg per day for 15 days, by gastric gavage, n = 15). Systolic blood pressure was determined before and after antioxidant treatments by the tail-cuff method. At 16 weeks of age, the rats were used for the study of microvascular reactivity and intravital fluorescence microscopy. Intrauterine undernutrition induced hypertension, and vitamins C or E treatments reduced the blood pressure levels. The decreased acetylcholine and bradykinin-induced vasodilation was restored in the vitamin-treated rats. These effects were associated with decreased vascular superoxide anion concentration. The results show that vitamins C and E reduce oxidative stress and high blood pressure levels, and improve vascular function in intrauterine-undernourished rats.
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PMID:Vitamins C and E improve endothelial dysfunction in intrauterine-undernourished rats by decreasing vascular superoxide anion concentration. 1288 24

The long-term effects of amlodipine, a calcium channel blocker, were examined in patients with moderate to severe hypertension. Eighteen never-treated patients with moderate to severe essential hypertension (49 +/- 8 years) were studied. In all patients, forearm blood flow (FBF) was measured by plethysmography before and 6 months after amlodipine treatment. Endothelium-nondependent and endothelium-dependent vasodilations were assessed by intrabrachial infusion of sodium nitroprusside (SNP) and acetylcholine (ACh), respectively. FBF modification by vitamin C, an oxygen radical scavenger, was also assessed under ACh infusion. The results were compared with those of 13 normal subjects. Blood pressure was significantly lowered (from 176 +/- 17/97 +/- 13 to 144 +/- 12/82 +/- 10 mm Hg) after treatment (P < 0.01). Forearm vascular resistance was increased in the hypertensive patients before treatment; however, it was normalized after treatment during SNP infusion and was improved during ACh infusion. Since vitamin C improved FBF under ACh infusion both before and after the amlodipine treatment, it is suggested that the production of free radicals was not canceled by amlodipine. The analysis of heart rate variability showed that amlodipine does not activate sympathetic nerve function. Therefore, amlodipine is effective in lowering blood pressure associated with the improvement of vascular function, and is suggested to be an effective antihypertensive agent for patients with moderate to severe hypertension.
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PMID:Amlodipine improves vascular function in patients with moderate to severe hypertension. 1288 35

Experimental data suggest that oxidative stress might be enhanced in hypertension and contribute to platelet activation. We hypothesized that both oxidative stress and platelet activation could be related to the clinical characteristics of hypertensive patients. The urinary excretion of 11-dehydrothromboxane (TX) B2, reflecting in vivo platelet activation, was measured in 75 patients with mild to severe essential hypertension and 75 pair-matched, healthy controls. The urinary excretion of 8-iso-prostaglandin (PG) F2alpha was determined as an index of in vivo lipid peroxidation. Urinary 11-dehydro-TXB2 was significantly higher in essential hypertensives compared with controls. Although no statistically significant difference in urinary 8-iso-PGF2alpha was observed between patients and controls, plasma vitamin C was lower and plasma homocysteine higher in hypertensive patients than in controls. Both urinary 11-dehydro-TXB2 and 8-iso-PGF2alpha were higher in patients with advanced hypertensive retinopathy compared with patients without retinopathy. Multivariate linear regression analysis identified urinary 8-iso-PGF2alpha, plasma fibrinogen, homocysteine, and vitamin E as the only variables independently correlated with urinary 11-dehydro-TXB2. Logistic regression analysis showed that high urinary 8-iso-PGF2alpha, plasma fibrinogen, and homocysteine, as well as low plasma vitamin E, advanced retinopathy, elevated diastolic blood pressure, and the absence of antihypertensive treatment, were predictors of high urinary 11-dehydro-TXB2. We demonstrated increased oxidative stress and persistent platelet activation in essential hypertensives with advanced vascular lesions. These findings might help identify hypertensive patients who are at increased risk of cardiovascular events and who might benefit from long-term antiplatelet therapy.
Hypertension 2004 Jan
PMID:Determinants of platelet activation in human essential hypertension. 1465 53

By breeding and feeding salt to spontaneously hypertensive rats (SHR) continuously over a long period (until 60 wk old), rats with systolic blood pressures (SBP) of over 270 mmHg were prepared. It was studied whether or not supplying large amounts of vitamin C (200 mg/rat/d) over this period might bring any beneficial effect to blood pressure. Moreover, physico-chemical studies were performed to measure the components and enzymes in the blood and urine at 53 and 60 wk-old, and biochemical studies on vitamin C were also carried out in this experiment. Male (14 rats: 7 wk-old, 100-105 g) and female (15 rats: 7 wk-old, 95-100 g) SHR were divided into three groups and bred continuously for 53 wk. The A group rats were given salt (2.5 g/100 g of diet), the B group rats were given salt and vitamin C (500 mg/100 mL of drinking water), and the C group rats were controls. The results showed almost the same tendencies between male and female rats. The body weights of the SHR in groups A and B were slightly lower than group C. The amount of food intake in groups A and B was almost the same as group C. The amount of water intake was, in the order from highest to lowest, group A, B and C. The SBP of group A rats exhibited the highest value among the three groups. The SBP of group B rats given vitamin C simultaneously with the salt resulted in a low blood pressure level close to that of the controls (group C). Furthermore, the DBP (diastolic blood pressure) also reflected the antihypertensive effect of vitamin C as well. The heartbeat of the rats was highest in group A, and was comparable to the value in the rats receiving vitamin C simultaneously with salt. For the tests on occult blood and protein in the urine, group A rats showed strong positive reactions, whereas the group B and C rats had decreased results for both tests. The organ weights of the liver, stomach, spleen, adrenal gland and kidneys per 100 g rat body weight were not different among the three groups. The values for the bilirubin content, and the enzyme activities of ALT and AST in the blood showed to be the highest in the male rats of group A. The values from the group B rats decreased near to the normal value like the control group. Vitamin C was found to decrease the blood pressure in SHR, and also to work effectively to protect liver and kidney functions even under the condition of very high blood pressure, as high as 250 mmHg.
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PMID:Effects of vitamin C on high blood pressure induced by salt in spontaneously hypertensive rats. 1470 3

Endothelial dysfunction might be related to an increase in superoxide anion production in patients with hypertension, hypercholesterolemia, diabetes mellitus, and heart failure. Studies in animal models indicate that angiotensin II increases superoxide anion production by vascular tissues. We examined whether angiotensin II attenuates endothelium-dependent vasodilation via an increase in superoxide anion production in human forearm vessels in vivo. Forearm blood flow was measured in 23 healthy young men. We examined forearm vasodilator responses to an intra-arterial infusion of acetylcholine (4, 8, and 16 microg/min) and sodium nitroprusside (0.8, 1.6, and 3.2 microg/min) before and during an intra-arterial infusion of anglotensin II (n=8), angiotensin II plus vitamin C (n=8), and vitamin C alone (n=4). Angiotensin II attenuated the forearm vasodilatory response to acetylcholine (p<0.05), and this attenuated response was abolished by vitamin C. Angiotensin II did not alter the forearm vasodilatory response to sodium nitroprusside, and vitamin C infusion did not affect the forearm vasodilatory response to either acetylcholine or sodium nitroprusside. The forearm vasodilator response to acetylcholine did not change during infusion of norepinephrine (n=3), which reduced forearm blood flow to a degree similar to that by angiotensin II infusion. These results suggest that angiotensin II attenuates endothelium-dependent forearm vasodilation, and vitamin C improves this impairment. Thus, angiotensin II likely attenuates endothelium-dependent vasodilation via an increase of superoxide anion production in the human forearm in vivo.
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PMID:Vitamin C improves attenuated angiotensin II-induced endothelium-dependent vasodilation in human forearm vessels. 1471 37

Hypertension increases oxidative stress, which can impair myocardial microvascular function and integrity. However, it is yet unclear whether long-term antioxidant intervention in early hypertension would preserve myocardial perfusion and vascular permeability responses to challenge. Pigs were studied after 12 weeks of renovascular hypertension without (n=8) or with daily supplementation of antioxidants (100 IU/kg vitamin E and 1 g vitamin C, n=6), and compared with normal controls (n=7). Myocardial perfusion and microvascular permeability were measured in vivo by electron beam computed tomography before and after 2 cardiac challenges (intravenous adenosine and dobutamine). Basal left ventricular muscle mass was also obtained. Mean arterial pressure was significantly increased in both groups of hypertensive animals (without and with antioxidants, 123+/-9 and 126+/-4 mm Hg, respectively, versus normal, 101+/-4 mm Hg; both P<0.05), but muscle mass was not different among the groups. The impaired myocardial perfusion response to adenosine observed in hypertensives (normal, +51+/-14%; P<0.05 versus baseline; hypertension, +14+/-15%; P=0.3 versus baseline) was preserved in hypertensive pigs that received antioxidants (+44+/-15%; P=0.01 compared with baseline). Long-term antioxidant intervention also preserved subendocardial microvascular permeability responses in hypertension. On the other hand, antioxidant intervention had little effect on the hypertension-induced myocardial vascular dysfunction observed in response to dobutamine. This study demonstrates that the impaired myocardial perfusion and permeability responses to increased cardiac demand in early hypertension are significantly improved by long-term antioxidant intervention. These results support the involvement of oxidative stress in myocardial vascular dysfunction in hypertension and suggest a role for antioxidant strategies to preserve the myocardial microvasculature.
Hypertension 2004 Feb
PMID:Long-term antioxidant intervention improves myocardial microvascular function in experimental hypertension. 1471 62

To examine the effect of vitamin C on blood flow in diabetic dental pulp, the animal model of streptozotocin (STZ)-induced diabetic rats (i.v. injection of STZ 55 mg/kg BW) was used. Male Sprague-Dawley rats weighing 200-250 g were divided into 3 groups: non-diabetes (CON), diabetes (STZ), and diabetes supplemented by vitamin C (STZ+Vit C). Vitamin C was supplemented by drinking water (1 g/l). At 12 weeks (wks) and 24 wks after the STZ injection, the laser Doppler flow-meter (Model ALF 21, USA) was used to measure pulpal blood flow (PBF) while the animals were anesthetized with sodium pentobarbital (50 mg/kg BW). The experimental results showed that at 12 and 24 wks after the STZ injection, hyperglycemia hypertension and loss of body weight were significantly developed. Simultaneously, decreased plasma vitamin C level was demonstrated significantly in STZ rats. The reduction of pulpal blood flow (PBF) in the lower incisors was observed in STZ rats at both monitored time points. Interestingly, the supplementation of vitamin C for 24 wks restored PBF. In conclusion, the present study demonstrated that long-term supplementation of vitamin C, a natural antioxidant, could markedly prevent the diabetic-induced reduction in PBF.
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PMID:The effect of long-term supplementation of vitamin C on pulpal blood flow in streptozotocin-induced diabetic rats. 1472 56

Coronary syndromes are induced by atherosclerosis which results from lipid deposit as well as inflammatory cells in vascular walls triggered by oxidative modification of LDL cholesterol. Treatment with antioxidant vitamins (vitamin C and E) has no evident effect on coronary events whereas aspirin and statins treatments result in a 25 to 30% reduced rate of fatal and non fatal myocardial infarction in primary and in secondary prevention trials. Both drugs are highly recommended in secondary prevention. In primary prevention they are useful and cost effective if the estimated risk of coronary event is 1.5% per year or higher. They are not cost-effective if this risk is 0.6% per year or less. With aspirin there is a 1.5 fold increase of hemorrhagic stroke and a 2 fold increase of gastrointestinal hemorrhage. Aspirin is less efficient in younger patients (< 50 years of age), in those with high blood pressure (> 145 mmHg) and those with low serum hsCRP (< 1 mg/l.). Statins are well tolerated and they could reduce not only C-V and global mortality but also the risk of stroke and of macular degeneration. They could also delay the occurrence of diabetes and kidney failure. Folate administration can lower elevated serum homocysteine level, which is a risk factor for C-V and Alzheimer's disease. However the clinical benefit resulting from folate treatment must still be demonstrated.
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PMID:[Prevention of cardiovascular and degenerative diseases: I. Aspirin, statins, or vitamins?]. 1509 4

The goal of this review is to evaluate the efficacy of commonly available dietary supplements in the treatment of hypertension, using the average blood pressure reduction achieved with the implementation of lifestyle modifications as a standard. For this reason, the authors focus on the antihypertensive potential of these agents rather than pharmacology, pharmacokinetics, adverse effects, or supplement-drug interactions. For the purpose of this review, dietary supplements are defined as exhibiting some evidence of benefit if a systolic blood pressure reduction of 9.0 mm Hg or greater and/or a diastolic blood pressure reduction of 5.0 mm Hg or greater has been observed in previously published, peer-reviewed trials. These defining limits are based on the average blood pressure reduction associated with the implementation of certain lifestyle modifications. Agents with some evidence of benefit include coenzyme Q10, fish oil, garlic, vitamin C, and L-arginine.
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PMID:The natural treatment of hypertension. 1513 3

Convincing evidence suggests that blood redox changes play a role in the development of various cardiovascular disorders including hypertension. Nutritional antioxidants have been suggested to play a role in cardiovascular disease prevention. In this study, we investigated in vivo changes in rat arterial blood pressure induced by acute exposition to an increased load of peroxyl radicals and by the administration of selected antioxidants after chemically induced oxidative stress. Hydrosoluble and liposoluble peroxyl radicals, generated by 2,2'-azobis-(2-amidinopropane) dihydrochloride and 2,2'-azobis 2,4-di-methylvaleronitrile, induced a dose-dependent decrease in rat blood pressure. All antioxidants tested (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid, vitamin C, glutathione and dithiothreitol) returned peroxyl radical-induced hypotension to normal. Of the various antioxidants tested, glutathione was the most effective in restoring blood pressure after peroxyl radical generation. Treatment of rats with a thiol-chelating agent (N-ethylmaleimide) and an oxidizing agent (5,5'-dithiobis-2-nitrobenzoic) inhibited peroxyl radical-mediated hypotension. Our results suggest that acute exposition to peroxyl radicals have a hypotensive effect on blood pressure and that thiols play an active role in the redox regulation of blood pressure. Other experiments are needed to clarify the role played by oxidative potentials on blood pressure and the mechanism of action of nutritional antioxidants.
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PMID:Effect on rat arterial blood pressure of chemically generated peroxyl radicals and protection by antioxidants. 1515 37


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