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

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

Patients with diabetes mellitus have an increased risk for coronary artery disease due to hyperglycemia, hypertension, dyslipidemia, and other risk factors. The diabetic dyslipidemia in these patients is characterized by moderately high levels of (1) serum cholesterol and triglycerides; (2) small, dense low-density lipoprotein (LDL) particles; and (3) low high-density lipoprotein (HDL) cho-lesterol concentrations. Recent clinical trials have demonstrated the benefits of cholesterol-lowering therapy in both diabetic and nondiabetic patients, thus supporting aggressive treatment of diabetic dyslipidemia for coronary artery disease prevention. A 3-step approach is recommended for the treatment of diabetic dyslipidemia. First, modification of diet and lifestyle, including decreased intakes of cholesterol, cholesterol-raising fats, and total energy, and increased physical activity should be advised. Second, good glycemic control should be achieved with diet and hypoglycemic drugs, if needed. Third, lipid-lowering drugs should be used, if necessary. Non-HDL cholesterol levels, which include both very-low-density lipoprotein (VLDL) and LDL cholesterol, should be the target of cholesterol-lowering therapy. The use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (the "statins") has become the first-line drug therapy for diabetic dyslipidemia. Bile acid sequestrants are effective cholesterol-lowering agents in normotriglyceridemic patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients with severe hypertriglyceridemia may require fibric acids or n-3 polyunsaturated fatty acids. Nicotinic acid worsens hyperglycemia; therefore, it should be avoided in most cases. The efficacy and safety of estrogen-replacement therapy in postmenopausal women with diabetes needs to be determined. The combination of two lipid-lowering agents may be appropriate for some NIDDM patients but should be used judiciously.
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PMID:Treatment of diabetic dyslipidemia. 952 14

Subjects with diabetes have a greatly increased risk of CHD, which is only partially related to their elevated glucose. Other factors such as insulin resistance and dyslipidemia are likely to be important. The type of dyslipidemia that is most characteristic of type 2 diabetic subjects is elevated triglycerides and decreased HDL cholesterol levels, although all lipoproteins have compositional abnormalities. Surprisingly few good prospective studies of lipoprotein levels in relation to CHD have been done in diabetic subjects. Available studies suggest that low HDL cholesterol may be the most important risk factor for CHD in observational studies. In studies in which total cholesterol and triglyceride were done, cholesterol and triglycerides were risk factors for CHD, although triglycerides were often a stronger predictor. However, the strength of triglyceride as a risk factor for CHD may depend partially on its association with other variables (e.g., hypertension, plasminogen activator inhibitor 1 [PAI-1], etc.). In clinical trials in diabetic subjects, LDL reduction with statins has led to significant reductions in CHD incidence. In addition, overall mortality was reduced with statin therapy, although the results were not statistically significant. Gemfibrozil has led to reductions in CHD incidence in diabetic subjects, although the results were not statistically significant perhaps because of low sample size. Regarding lipoproteins and CHD risk in diabetic patients, the very positive results of statin trials point to LDL cholesterol being more important than previous realized. Apparently, having a borderline high LDL cholesterol (between 130 and 160 mg/dl) in a diabetic patient is equivalent to a much higher LDL cholesterol in terms of CHD risk for a nondiabetic subject. Therefore, the primary target of therapy in diabetic patients is lowering LDL cholesterol (or possibly, non-HDL cholesterol). Statins are the preferred pharmacological agent in this situation. Once LDL cholesterol levels have been lowered, attention can be given to treatment of residual hypertriglyceridemia and low HDL. The goal here is weight reduction and increased exercise. However, for selected patients, combining a fibric acid (or low-dose nicotinic acid) with a statin also can be considered. Reduction of LDL levels should take priority over reduction of triglycerides in combined hyperlipidemia because of the proven safety of the statin class of drugs as well as greater reduction in CHD incidence.
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PMID:Management of dyslipidemia in adults with diabetes. 953 88

Disorders in the system of blood aggregation state control (BASC) reflects the severity of OPH-gestosis (edema, proteinuria, hypertension). The duration of the therapeutic effect of the applied antithrombotics has not been studied essentially. The parameters and duration of the effective responses in the BASC system after a single dose of aspirin, curantyl, and nicotinic acid were studied in 45 females with OPH-gestosis of moderate severity. The deaggregation effect of aspirin lasted 48 h, that of nicotinic acid persisted for 7 h., the effect of curantyl developed in 72 h. and lasted 24 h. The prescription of individually selected and controlled doses of activators of fibrinolysis and deaggregants makes it possible to abolish disorders of the BASC system in pregnant females with OPH-gestosis of moderate severity.
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PMID:[The duration of the action of a single dose of aspirin, kurantil and nicotinic acid during pregnancy complicated by EPH gestosis]. 1043 46

Previous investigations have identified focal areas of alveolar bone tenderness, increased mucosal temperature, abnormal anesthetic response, radiographic abnormality, increased radioisotope uptake on bone scans, and abnormal marrow within the quadrant of pain in patients with chronic, idiopathic facial pain. The present case reports a 53-year-old man with multiple debilitating, "idiopathic" chronic facial pains, including trigeminal neuralgia and atypical facial neuralgia. At necropsy he was found to have numerous separate and distinct areas of ischemic osteonecrosis on the side affected by the pains, one immediately beneath the major trigger point for the lancinating pain of the trigeminal neuralgia. This disease, called NICO (neuralgia-inducing cavitational osteonecrosis) when the jaws are involved, is a variation of the osteonecrosis that occurs in other bones, especially the femur. The underlying problem is vascular insufficiency, with intramedullary hypertension and multiple intraosseous infarctions occurring over time. The present case report illustrates the extreme difficulties involved in the diagnosis and treatment of this disease.
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PMID:Maxillofacial osteonecrosis in a patient with multiple "idiopathic" facial pains. 1053 67

The 'metabolic syndrome' is a special clinical entity characterized by upper body segment obesity (android obesity), together with one or more of a constellation of metabolic disorders that includes glucose intolerance, which may amount to frank diabetes mellitus, hypertension, cardiovascular lesions, hyperuricemia, and dyslipidemias (hypercholesterolemia, hypertriglyceridemia and reduced serum HDL). Recently, lipoprotein (Lp) (a) proved to be a new member in this syndrome. Lp(a) has the distinctive feature of containing apolipoprotein (a), which is a glycoprotein linked to apo B100, and has a similarity to plasminogen; it is also structurally related to LDL. Lp(a) is a macromolecular complex which is genetically determined, and has been identified as an independent risk factor for premature coronary artery disease (CAD). It is elevated in diabetic and non-diabetic android obese subjects, and aggravates the atherogenic effect of diabetes mellitus. Lp(a) is poorly influenced either by dietary measures or by hypolipidemic drugs. Unfortunately, few pharmacologic agents, such as niacin, nicotinic acid, sex hormones (estrogen and testosterone), alcohol and neomycin, affect Lp(a).
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PMID:Lipoprotein (a) in android obesity and NIDDM: a new member in 'the metabolic syndrome'. 1066 39

The hypertriglyceridemia attends the physiopathology of the atherosclerosis by various mechanisms: association of low levels of high density lipoprotein-cholesterol (HDL-c), modification of quality of low density lipoprotein-cholesterol (LDL-c), influence on hemostatic processes, association with other hazard's factors (obesity, hypertension, etc.). The hypertriglyceridemia distinguishes in primary and secondary. In primary forms the origin is essentially genetic, while the secondary ones are metabolic consequence of various pathologies (renal, thyroid, diabetes mellitus etc.). The hypertriglyceridemia's treatment is founded on a correct feeding and/or on eventual use of drugs. Apart from the secondary forms, in which is obligatory to treat at first the basal disease, the pharmacological therapy of the hypertriglyceridemia is suggested only in resistant cases to alone dietetic therapy and overall in presence of other factors of atherothrombotic hazard. The most utilized drugs are: omega-3 fatty acids, the nicotinic acid and its derivatives, the fibrates and the statins. The stronghold of alpha-glucosidases inhibitors is the acarbose. It reduces the biosynthesis of very low density lipoproteins (VLDL) by the reduction of substrata with an improvement of glucidic metabolism. Atorvastatin and cerivastatin develop a greater action to reduce serum levels of triglycerides as to the foregoing ones because of the better selectivity of receptor binding, the greater halflife and inhibition of the apolipoprotein's B100 synthesis.
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PMID:[Treatment of hypertriglyceridemia. Current aspects]. 1093 25

Numerous studies report strong associations between hyperhomocysteinemia and premature atherosclerotic vascular disease. Causes of hyperhomocysteinemia are hereditary heterozygous or, in very rare cases, homozygous defects, and quite frequently a lack of the coenzymes B6 and B12 and the cosubstrate folate. Lifestyle factors, age, sex, acute and chronic illness, vitamin deficiency and certain drugs may elevate homocysteine concentrations. Vitamin B supplementation, especially folic acid, is an effective treatment of hyperhomocysteinemia. Clinical trials are required to confirm the potential benefit of lowering homocysteine in regard of the development and progression of atherosclerotic vascular disease. The relevance of hyperhomocysteinemia as a risk factor for atherosclerosis, in contrast to the classical triad of risk factors, namely hypercholesterolemia, smoking and hypertension, is still unknown. Furthermore, a lack of standardized analytical methods for the determination of both homocysteine and blood folate renders the evaluation of studies and clinical data difficult. Therefore, at present, diagnosis and treatment is only recommended in high-risk patients (strong family history of premature atherosclerosis or arterial occlusive disease, especially in the absence of other risk factors, as well as in members of their families) with hyperhomocysteinemia.
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PMID:Homocysteine--relevant for atherogenesis? 1095 70

Insulin resistance and hyperinsulinaemia are associated with hypertension although a causative relationship has not been established. The aim of this study was to determine whether a short term reduction in insulin sensitivity induced by nicotinic acid treatment (NA) would alter blood pressure. The study was a double-blind randomised placebo-controlled cross-over study. Seven healthy volunteers, three males and four females were randomised to placebo or NA 500 mg daily for 7 days then 1 g daily for a further 7 days. Hyperinsulinaemic euglycaemic clamp, indirect calorimetry, 24-h ambulatory blood pressure monitoring (ABPM) and forearm blood flow measurement (FABF) were performed at day 14 of each treatment phase. NA significantly reduced the glucose infusion rate required to maintain euglycaemia in all subjects (placebo vs NA; 31.5+/-4.2 vs. 26.2+/-4.6 micromol/kg/min, P = 0.002) associated with a decrease in non-oxidative glucose disposal. NA did not significantly alter 24-h mean systolic or diastolic blood pressure. Fasting glucose, insulin and non-esterified free fatty acid (NEFA) levels remained unchanged, energy expenditure and substrate oxidation were not altered by NA. These results suggest a short term reduction in insulin sensitivity with NA is not accompanied by a change in blood pressure. This may relate to the short duration of treatment, to a dissociation between insulin resistance and hypertension or to other homeostatic mechanisms which prevent blood pressure rising in subjects not predisposed to hypertension.
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PMID:Effects of nicotinic acid on insulin sensitivity and blood pressure in healthy subjects. 1098 May 88

Patients with type 2 diabetes (formerly known as non-insulin-resistant diabetes) have a significantly increased risk of developing cardiovascular disease. Once clinical cardiovascular disease develops, these patients have a poorer prognosis than normoglycemic patients. By inducing endothelial changes, hyperglycemia contributes directly to atherosclerosis. Type 2 diabetes is also associated with atherogenic dyslipidemias. This form of diabetes, or the precursor state of insulin resistance, commonly occurs as a metabolic syndrome (formerly known as syndrome X) consisting of hypertension, atherogenic dyslipidemia and a procoagulant state, in addition to the disorder of glucose metabolism. All cardiovascular risk factors except smoking are more prevalent in patients with type 2 diabetes. In addition to exercise, weight control, aspirin therapy and blood pressure control, therapy to modify lipid profiles is usually necessary. The choice of agent or combination of statin, bile acid sequestrant, fibric acid derivative and nicotinic acid depends on the lipid profile and characteristics of the individual patient.
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PMID:Attenuating cardiovascular risk factors in patients with type 2 diabetes. 1114 70


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