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

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.
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PMID:Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats. 50 48

Coffee as a rule develops stimulating effects on the central nervous system, heart and circulation which are mainly caused by caffeine. In certain cases coffee may also have a sedative effect and sometimes even it is useful to fall asleep quickly. Furthermore coffee may be advantageous in the treatment of some functional disorders caused by lacking of dopamine, because coffee is able to increase the dopamine formation in brain. Concerning the effects of coffee in the gastrointestinal-tract and liver-bile system caffeine is only of secondary importance. Hereby certain roasting substances, possibly also chlorogenic acid or caffeic acid should be responsible for the stimulating effects observed in these organs. These stimulating effects could be caused whether directly or indirect e.g. by liberating gastrin or other gastrointestinal hormones. Vitamin niacin, which is formed in greater amounts from trigonelline during the roasting process, may also be important from the nutritional standpoint. Therefore coffee may be prescribed as a true drug in cases of deficiency in vitamin niacin or also in the pellagra disease. By extensive epidemiological studies performed lately it could be demonstrated that there exists no correlation between coffee consumption and certain risk factors as hypertension, heart infarction, diabetes, gout or cancer diseases. Furthermore there was no evidence that coffee or its caffeine content are able to induce genetic alterations or even malformations.
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PMID:[Coffee and health]. 60 27

1. Oral administration of DL-alpha-tocopheryl nicotinate (EN) (0-04 or 0-2 mmol day-1 kg-1) or DL-alpha-tocopharyl acetate (EA) (0-2 mmol day-1 kh-1) delayed the progress of hypertension in unilaterally nephrectomized rats, which were treated with deoxycorticosterone and salt, and in genetically hypertensive rats (SHR) which were given sodium chloride solution. Suppression of body weight gain, incidence of pneumonia and mortality were reduced by treatment with EN or EA. 2. Severe hypertension in old SHR (9 months) further progressed, when drinking water was replaced by sodium chloride solution, and four out of ten of these animals died of cerebral haemorrhage during 4 weeks. The administration of EN or EA prevented the increase in blood pressure and incidence of stroke.
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PMID:Anti-hypertensive action of DL-alpha-tocopharyl esters in rats. 107 97

The influence of 7-[2-hydroxy-3-(N-2-hydroxyethyl-N-methylamino)propyl]-1, 3-dimethyl-xanthine-pyridine-3-carboxylate (xantinol nicotinate, Complamin) on brain metabolism was studied in the following test models: 1. determination of glucose-14C permeation in rats with experimental nephrogenic hypertension; 2. determination of the intercerebral ATP-concentration in ischaemic rats; 3. determination of the adenosine triphosphate (ATP) pool in healthy rats; 4. evaluation of the incorporation rates of 32Pi-isotope into the adenosine phosphates of the rat brain. The results of these studies show, that the reduced glucose permeation rates in rats with nephrogenic hypertension can be normalized by xantinol nicotinate above values of controls. In hypoxemic rats it could be shown, that xantinol nicotinate antagonizes the decrease of the intracerebral ATP-concentration by 50%. The investigation of the ATP-pool resulted in a significant increase of the ATP level in the brain tissue about 35% at maximum. This increase of the ATP-concentration continues up to 4 h following a single oral administration of xantinol nicotinate. The determination of the incorporation rates of 32Pi-isotope showed that only small amounts of radioactivity were measured in the AMP-fraction in controls as well as in xantinol nicotinate treated rats. Further phosphorylation steps of adenosine monophosphate (AMP) to adenosine diphosphate (ADP) and ATP, however, are considerably activated by xantinol nicotinate, whereby maximum labelling rates of the ADP were found already 15 min after dosing. Maximum 32Pi-incorporation rates of the ATP-fraction were measured 30 min following administration of the tracer and of xantinol nicotinate, respectively.
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PMID:[Effect of xanthinol nicotinate on brain metabolism in rats]. 668 47

Lipoprotein(a) [Lp(a)] consists like the low-density-lipoprotein (LDL) in the structure protein apolipoprotein B, but is additionally connected with apolipoprotein(a), which is highly homologous to plasminogen. The physiological function of Lp(a) is yet not entirely clear. Lp(a) is established to be an independent factor in the genesis of atherosclerosis however. With occurrence of high Lp(a) Lp(a) plasma levels and other atherogenous risk factors at the same time a potentiation of their effects on genesis of atherosclerosis is observed. Unfortunately the therapeutic possibilities of counteracting the high atherogenicity of Lp(a) are still limited, because LDL apheresis as the only known effective technique today cannot be applied in all cases. In several studies it has been shown, that Lp(a) concentrations can be reduced mainly by long term treatment with lipid-lowering sustained-release bezafibrate, ACE-inhibitor fosinopril, alpha-tocopheryl-nicotinate and N-acetylcysteine. Because of the synergistic effects of atherogenous risk factors patients with high Lp(a) concentrations should avoid additional risk factors such as hypertension, smoking, diet increasing LDL, etc.
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PMID:[The significance of lipoprotein(a) in assessment of risk for atherosclerosis]. 783 88

No differences were found in the rate of metabolism of vitamins B1, B2, B6 and niacin either in healthy persons or in patients with duodenal ulcer, hypertension of the 2nd degree and with ischemic heart disease as shown by excretion of riboflavin, 4-pyridoxylic acid, 1-methyl nicotinamide and thiamin with urine which correlated with concentration of these vitamins and their coenzyme forms in blood plasma and erythrocytes. Dependence of these vitamins excretion with urine on their concentration in blood and the vitamins content in food appear to demonstrate similar consumption of vitamins B in the persons studied; at the same time, evaluation of the vitamins consumption in the patients with these forms of pathology should be performed using the criteria suitable for healthy persons. Dissimilar rates of metabolism of these vitamins described in literature might be related to differences in nutrition as well as to the use of nonspecific techniques for estimation of the vitamins. Besides, initial consumption of vitamin B2 was not sometimes considered, but deficiency in riboflavin caused considerable impairments of vitamin B6 and niacin metabolism.
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PMID:[B group vitamin metabolism in duodenal ulcer disease, hypertension, and ischemic heart disease]. 816 Apr 30

Hypertension and diabetes appear to increase coronary heart disease risk in part by causing an abnormality in lipid metabolism. Most affected are patients with familial dyslipidemic hypertension (FDH) and noninsulin-dependent diabetes mellitus (NIDDM). The lipid disorders most often encountered in these patients are increased levels of triglycerides, very low-density lipoprotein (VLDL) cholesterol, and small, dense low-density lipoprotein (LDL) cholesterol, and low levels of high-density lipoprotein (HDL) cholesterol. These abnormalities appear to result from increased hepatic secretion of VLDL particles due to increased concentrations of free fatty acids and glucose, reduced VLDL clearance due to reduced activity of lipoprotein lipase, and reduced LDL clearance due to glycosylation of ligand proteins. Treatment of the dyslipidemia associated with FDH should follow the guidelines from the National Cholesterol Education Program. Treatment in men and women with NIDDM should be considered when LDL cholesterol levels are 130 mg/dl or above, triglyceride levels are 200 mg/dl or above, or non-HDL cholesterol levels are 160 mg/dl or greater. Aggressive lifestyle changes should be initiated first, including weight loss in obese patients, control of glucose levels in those with NIDDM, avoidance of antihypertensive drugs that may worsen lipid levels in patients with FDH, and eating a diet restricting saturated fat and cholesterol. Addition of lipid-altering drugs should be considered if such changes do not achieve effective lipid control. The agent should be tailored to the patient's lipid profile, in general by using bile acid resins, niacin, or reductase inhibitors to lower LDL cholesterol and gemfibrozil or niacin to lower triglycerides. Niacin should be avoided in patients with NIDDM.
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PMID:Understanding and treating dyslipidemia associated with noninsulin-dependent diabetes mellitus and hypertension. 836 60

Ingestion of sugars (sucrose, fructose, glucose) by various rat strains is associated with perturbations in the glucose/insulin system and higher systolic blood pressure (SBP). The association suggests causality, because alterations in insulin metabolism have been found in essential hypertension and many experimental forms of hypertension. To test the hypothesis that sugar-induced SBP elevation is secondary to perturbed insulin metabolism, we examined in 2 experiments effects of chromium and guar, substances known to affect insulin metabolism, on SBP of Spontaneously Hypertensive Rats (SHR). In both studies, sucrose compared to starch ingestion caused significant elevation of SBP; but addition of 2 chromium nicotinate complexes and guar prevented development of sugar-induced SBP elevations. The basal, genetic hypertension of the SHR was not affected by either nutrient. An additional finding in the first study was that sugar-consuming SHR supplemented with chromium had greater BW and increased organ weight (kidney, spleen, and liver) than nonsupplemented SHR. Accordingly, we have shown that two different mechanisms known to ameliorate insulin perturbations, use of chromium and guar, prevent sugar-induced SBP elevations. Since essential hypertension may be due to insulin perturbations and high dose chromium supplementation seems nontoxic, this may prove to be a useful means to lower blood pressure (BP) in some essential hypertensives, as well as diabetic hypertensives. Soluble fiber in the form of guar is also quite effective in favorably influencing sugar-induced SBP elevations.
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PMID:Effects of chromium and guar on sugar-induced hypertension in rats. 855 33

In a previous study, we found that oral chromium nicotinate overcame sucrose-induced hypertension in spontaneously hypertensive rats (SHR). Accordingly, we examined more chromium compounds to determine if others were more or less effective in regulating blood pressure (BP) of SHR. Since chromium is postulated to be an antioxidant, we also assessed the ability of different chromium compounds to alter free radical formation measured by determining thiobarbituric acid reactive substances (TBARS). The control group of SHR ingested a diet low in chromium, and 5 other groups ate the same diet with various chromium compounds added at 5 ppm-chloride, acetate, nicotinic acid-glycine-cysteine-glutamic acid (NA-AA), picolinate, and nicotinate. Following this, the rats were challenged with drinking water containing 5% and 10% w/v sucrose. Except for NA-AA, all chromium compounds inhibited the sucrose-induced elevation of systolic BP; and acetate, picolinate, and nicotinate chromium compounds lowered HbAIC below control. Only chromium acetate and nicotinate significantly lowered both hepatic and renal TBARS. Chromium picolinate lowered hepatic TBARS, and chromium chloride and NA-AA lowered neither. We conclude that chromium, rather than a specific ligand, plays a major role in ameliorating sucrose-induced BP elevations and can act as an antioxidant.
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PMID:Effects of different chromium compounds on blood pressure and lipid peroxidation in spontaneously hypertensive rats. 918 Dec 80

We studied endothelial function using the brachial artery ultrasound model in 100 subjects from the Armed Forces Regression Study, a placebo-controlled, angiographic regression trial in subjects with normal or modestly elevated low-density lipoprotein (LDL) cholesterol and low levels of high-density lipoprotein (HDL) cholesterol treated for 30 months with gemfibrozil and (if necessary) niacin and/or cholestyramine to raise HDL by 25% and lower LDL to < 110 mg/dl. Although the treatment group had highly significant improvements in LDL and HDL cholesterol, there was no difference between the 2 groups in flow-mediated dilation (treatment vs control 6.9 +/- 6.5% vs 6.3 +/- 7.3%) or nitroglycerin-induced dilation (12.4 +/- 9.6% vs 11.9 +/- 7.4%, all p = NS). Treatment and control subjects without a history of hypertension had flow-mediated dilation similar to that of a normal reference population (10.6 +/- 8.3% vs 8.4 +/- 4.5%), whereas subjects with a history of systemic hypertension had markedly impaired flow-mediated dilation that was not significantly improved with treatment (treatment vs control, 6.0 +/- 5.5% vs 4.3 +/- 5.9%, p = 0.2). Thus, nonhypertensive subjects with angiographic coronary disease and low HDL cholesterol had normal endothelial function in the brachial artery model. Patients with a history of hypertension had marked endothelial dysfunction despite blood pressure treated to normal levels, and this dysfunction is not attenuated by pharmacologic therapy for dyslipidemia.
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PMID:Effect of gemfibrozil +/- niacin +/- cholestyramine on endothelial function in patients with serum low-density lipoprotein cholesterol levels <160 mg/dl and high-density lipoprotein cholesterol levels <40 mg/dl. 938 93


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