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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.02 seconds)

The aim in treatment of hypertension is normalization of blood pressure. The impact of treatment of hypertension on the development of IHD depends not only on the treatment of hypertension but also on influencing other basic risk factors, i.e. hyperlipoproteinaemia and smoking. Treatment of hypertension can be and should be individual and depends on a) age, b) the level of hypertension, c) complications of hypertension and d) the presence of other diseases, in particular hyperlipoproteinaemia and diabetes mellitus. The treatment of choice in hyperlipoproteinaemia are calcium antagonists, prazosin, ACE inhibitors and beta-blockers with ISA. There is experimental evidence suggesting that calcium antagonists (in particular isradipine) but also beta-blockers suppress the progression of atherosclerosis and AGE inhibitors prevent the development of cardiac and vascular hypertrophy. Effective treatment leads to a decline in the mortality from cerebrovascular attacks--in the USA in the course of 20 years a decline by 60%--in Czechoslovakia so far the mortality from cerebrovascular disease did not change which indicates unfortunately a very poor control of hypertension in the population.
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PMID:[Treatment of hypertension and cardiovascular complications]. 182 87

AGE-RELATED CARDIOVASCULAR CHANGES: Age-related changes in vascular structure and function may contribute to isolated systolic hypertension and target-organ damage. These include cardiac hypertrophy, systolic as well as diastolic dysfunction, congestive heart failure, coronary artery disease, cardiac arrhythmias, cerebrovascular diseases, peripheral vascular diseases and renal insufficiency. POTENTIAL ADVANTAGES OF CALCIUM ANTAGONISTS IN THE ELDERLY: Dihydropyridine calcium anatagonists have been advocated as first choice agents for the treatment of hypertension in the elderly on the grounds that (1) they may be more active in lowering blood pressure because of the predominantly low renin status in elderly hypertensives, (2) they may be better tolerated because side effects related to the activation of the sympathetic system may be less frequent because of attenuation of baroflexes during ageing and (3) they may have beneficial effects on a variety of concomitant cardiovascular diseases which are frequently present in the elderly. These assumptions, however are not always proven in clinical practice. ADVANTAGES OF NICARDIPINE: Additional to its potent vasodilatator action, nicardipine has anti-ischemic effects in both the coronary and the cerebral circulation, including antiplatelet and hemorrheological effects, and protection at ther cellular level against calcium overload and ischemia. The results of a large number of studies in cerebrovascular insufficiency suggest that nicardipine, may favourably affect the cerebral circulation and may improve the patient's cognitive function. Nicardipine may decrease left ventricular mass by about 4-12% and may reduce both the frequency and the severity of arrhythmias. The anti-anginal effects of nicardipine are well established. The drug is also able to decrease the progression of new atherosclerotic lesions in coronary arteries and is consequently potentially beneficial in elderly hypertensives with coronary artery disease. Nicardipine has no clinically significant negative inotropic effect. Nevertheless, in congestive heart failure, the use of calcium antagonists is usually not recommended because of the lack of clinical benefit and of possible harmful effects, including sympathetic and renin-angiotensin system stimulation. Although kidney protection may be provided by a strict and long-term control of blood pressure, the effects of nicardipine on long-term protection of renal function are not clear at present. RECENT CONTROVERSY CONCERNING SHORT-ACTING CALCIUM ANTAGONISTS: Much-debated recent case-control studies suggest that hypertensive patients treated with short-acting calcium antagonists may have an increased incidence of myocardial infarction and possibly of cardiovascular and total mortality. However, only well designed prospective comparative trials can answer this question.
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PMID:Concomitant diseases in elderly hypertensives: the position of nicardipine. 912 Jun 65

The development of extensive atherosclerosis of major arteries of the heart, brain, and lower extremities is a particularly frequent problem in elderly individuals and is responsible for the majority of the cardiovascular morbidity and mortality in this population. Although the frequency and severity of this problem is well recognized, there has been relatively little investigation of the effects of aging on the development of atherosclerosis. Work by a number of investigators over the last 10-15 years has demonstrated that modifications of lipoproteins, resulting from oxidative stress, glycoxidation, formation of AGE, or other processes may play an important role in atherosclerosis. As described in this review, the aging process may enhance lipoprotein modification and atherosclerosis in several ways. Conditions such as hypertension, diabetes, and menopause all increase in frequency with advancing age and may contribute both directly and indirectly to lipoprotein modification and vascular injury.Additionally, in some studies of older animals and humans, there seems to be evidence for greater in vivo oxidative stress. Whether this is a specific consequence of aging and associated medical conditions, or related to differences in dietary fatty acid or antioxidant content or other lifestyle differences is currently unknown. One important consequence of this may be enhanced susceptibility of lipoproteins to oxidation. Additional study of lipoprotein modifications associated with aging is clearly needed, and may provide new insight and solutions to the common problem of atherosclerosis in the elderly.
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PMID:Lipoprotein modification and atherosclerosis in aging. 1081 8

Recent studies have shown that patients with high peritoneal transport characteristics have substantially increased morbidity and mortality. This finding is counter-intuitive, since HTs will a priori achieve higher clearances. There are many possible causes: increased protein losses with consequent hypoalbuminemia; poor ultrafiltration capacity causing fluid retention, ventricular hypertrophy and hypertension; increased glucose absorption leading to anorexia, hyperinsulinism, and local AGE formation; and the development of an atherogenic lipid profile. While common pathogenic causes of high peritoneal transport and atherosclerosis have been hypothesized, it is more likely that CAPD as currently practiced is unsuitable for HTs, who should be switched to HD or NIPD. Renal and peritoneal clearances have different clinical effects and should be assessed separately. Current measures of dialysis adequacy, such as total Kt/V, do not therefore describe the patient's clinical situation accurately and are insufficient.
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PMID:Pathogenic effects of a high peritoneal transport rate. 1083 80

Hypertension and diabetes mellitus represent increasing threats to the health of many populations. For reasons not completely understood, the prevalence of these diseases is higher in some ethnic groups than in others. The key to this puzzle may rest with the interplay of a defect of an enzyme-mediated process and the environment. Oxidative stress and impairment of synthesis or release of nitric oxide (NO) are being regarded as causative factors in the pathogenesis of hypertension, diabetes mellitus and atherosclerosis, among other conditions. Glucose-6-phosphate dehydrogenase (G6PD) deficiency has been overlooked as a cause of both oxidative stress and a decrease in the generation of nitric oxide (NO). G6PD generates nicotinamide adenine dinucleotide phosphate (NADPH), a co-factor in the synthesis of nitric oxide. There is impairment of the production of nitric oxide superoxide and hydrogen peroxide in G6PD-deficient granulocytes. In the polyol pathway, G6PD deficiency causes hyperglycemia, making more glucose available for the non-enzymatic production of advanced glycosylation end products (AGE's), which also causes an increase in superoxide anions and a quenching of nitric oxide. Currently, there are 200 million people worldwide with red cell x-linked chromosome defects who, with the persistent ingestion of refined carbohydrates, are at greater risk of developing hypertension or diabetes mellitus than those racial groups without the defect.
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PMID:G6PD deficiency: its role in the high prevalence of hypertension and diabetes mellitus. 1176 98

Arteriosclerosis, atherosclerosis and vascular calcification are causally related to the high morbidity and mortality of patients with chronic renal failure. Oxidative stress and carbonyl stress of uremia, dialysis procedure and/or intravenous iron therapy result in AGE (advanced glycation end-product), ALE (advanced lipoxidation end-product) and AOPP (advanced oxidation protein product) formation, favouring together with elevated CRP (C-reactive protein) levels the development of cardiovascular and cerebrovascular complications. Enhanced plasma levels of homocysteine and ADMA (asymmetric dimethylarginine) contribute to this process. In addition, in chronic renal insufficiency hyperphosphatemia and an enhanced calcium x phosphorus ion product are associated with the morbidity and mortality of the patients, particularly in the presence of fetuin deficiency. Phosphorus, AGEs and AOPPs, beside other factors, catalyze the conversion of vascular smooth muscle cells to osteoblast--like cells (particularly in the presence of monocytes/macrophages), resulting in bone matrix protein formation. Other risk factors, such as age, male sex, smoking, hypertension, diabetes, chronic inflammation, insulin resistance or dyslipidemia (enhanced non-HDL-cholesterol) also contribute to the atherosclerotic risk profile of the patient with chronic renal insufficiency. While there is growing understanding of the mechanisms involved in arteriosclerosis, atherosclerosis and vascular calcification in uremia, we are still missing effective therapeutic maneuvers for reduction of excess mortality in uremic patients.
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PMID:[Atherosclerosis and uremia: signifance of non-traditional risk factors]. 1277 74

All patients with CKD have multiple risk factors for CVD and CAD in particular. Some of these risk factors such as age and gender cannot be modified. Others such as diabetes and hypertension are not only CVD risk factors but are also the cause of the patient's CKD. Finally there are a group of risk factors such as disturbances of mineral metabolism and oxidative stress which are present either uniquely in or are exaggerated by renal failure. PD gives patients a more atherogenic lipid and lipoprotein profile, puts them at greater risk for AGE formation and usually causes hyperinsulinemia. All of these contribute to CVD risk. However, they can also achieve excellent blood pressure control, usually easily reach targets for anemia management and have continuous ultrafiltration allowing for the maintenance of good volume status, all of which will reduce risk for CVD. All treatable risk factors should be treated early in the development of CKD and should continue through their time on dialysis and after transplantation.
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PMID:Cardiovascular risk in peritoneal dialysis. 1280 Mar 47

Risk factors for cardiovascular disease, including high cholesterol, high homocysteine, hypertension and inflammation, increase the risk of dementia, including its most common form, Alzheimer's disease (AD). High cholesterol is also associated with elevated beta-amyloid (Abeta), the hallmark of AD. Oxidative damage is a major factor in cardiovascular disease and dementia, diseases whose risk increases with age. Garlic, extracted and aged to form antioxidant-rich aged garlic extract (AGE or Kyolic), may help reduce the risk of these diseases. AGE scavenges oxidants, increases superoxide dismutase, catalase, glutathione peroxidase, and glutathione levels, and inhibits lipid peroxidation and inflammatory prostaglandins. AGE reduces cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl-CoA reductase and is additive with statins in its action. Inhibition of cholesterol, LDL oxidation, and platelet aggregation by AGE, inhibits arterial plaque formation; AGE decreases homocysteine, lowers blood pressure, and increases microcirculation, which is important in diabetes, where microvascular changes increase heart disease and dementia risks. AGE also may help prevent cognitive decline by protecting neurons from Abeta neurotoxicity and apoptosis, thereby preventing ischemia- or reperfusion-related neuronal death and improving learning and memory retention. Although additional observations are warranted in humans, compelling evidence supports the beneficial health effects attributed to AGE in helping prevent cardiovascular and cerebrovascular diseases and lowering the risk of dementia and AD.
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PMID:Garlic reduces dementia and heart-disease risk. 1648 70

Retention of many substances takes place in the pathogenesis of uremic toxicity. There are almost 100 different molecules described and defined as uremic toxins. These substances are divided into three groups according to EUTOX group calssification. Small water soluble molecules with a molecular weight less than 500 D are included into the first group. Derivate of guanidines, purines, pyrimidines and methyloamines appeared in this group. There is also an unclassified subgroup with urea as a "classical" toxin which the real role in the uraemic syndrome is still discussed. Main symptoms caused by these molecules are digestive disturbances, neurological changes, hypertension etc. We can eliminate almost all of these toxins with standard methods used during dialysotherapy. Substances with a different molecular weight but connected with proteins determine the second group. AGE-s, phenol derivates, leptin and poliamines beside others create this group. There are many studies that have proved that these toxins cause hypertension, arteriosclerosis and shortened life time of hemodialysed patients. However, melatonin toxicity is not fully proved. Different types of renal replacement therapy are not valid to purify blood from protein-bound substances. Middle molecules are included into the third group, with a molecular weight higher than 500 D. There are cytokines, neuro-transmitters e.g. beta-endorphin, metencephalin and many others accounted into this group. One of them is the parathormon, well known and considered as "universal" toxin for several years. Middle molecules are causing very different effects. They are responsible for: anemia, arteriosclerosis, chronic inflammation and generally increase dialysed patient mortality. Toxic action of several molecules described below is still not proved; however there are some ongoing studies aimed to find pathophysiological links between old and new described uremic toxins.
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PMID:[Clinical and metabolic consequences of uremic toxicity]. 1708 Jul 44

New evidence about diabetic microangiopathy has enabled us to identify an integrated pathogenesis of diabetic complications, including classic metabolic pathways induced by hyperglycaemia, insulin-resistance, hyperinsulinaemia, hormonal alterations and growth factors. Oxidative stress is the most important cause of endothelial damage inducing leukocyte adhesion, altered coagulation and inflammation. Adhesion molecules are a marker of endothelial damage and a potential therapeutic target. Changes in the extracellular matrix induced by TGFbeta1 and lower levels of eparan-sulfate, increased thickness of basement membranes and loss of pericytes are early events of diabetic retinopathy and diabetic nephropathy. Capillary rarefaction produced by genetic factors or by fetal undernourishment contributes to the beginning of insulin-resistance and hypertension. Psychophysical tests, electroretinogram and evoked potentials show retinal functional alterations; fundoscopy and retinal fluorescein angiography show retinal anatomic alterations. The diagnosis of diabetic neuropathy is based not only on traditional neurological examination and electroneurograms, but also on neurothesiometry for sensory testing. Medical treatment of diabetic microangiopathy is based on control of glycaemia, lipemia and blood pressure using glytazones, ACE-inhibitors, angiotensin II receptor antagonists and statins. New knowledgeabout microangiopathy pathogenesis suggests potential drugs for its therapy (ruboxistaurin, AGE-inhibitors, angiopoietin-1 and anti-VEGF, etc.), not yet on sale.
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PMID:Diabetic microangiopathy: physiopathological, clinical and therapeutic aspects. 1791 58


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