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

Issuing from the present state of the influence of the basic nutritive substances (protein, fat, carbohydrates) and various nutritive factors discussed again and again (cholesterol, erucaic acid, sodium, calcium/magnesium quotient, pressor amines) on the development of the arteriosclerosis, the indididual factors of influence are critically evaluated. The investigations are getting under way, so that ascertained results are standing beside insufficiently claified or open problems, From the abundance of the observations conclusions are drawn which are of significance for practice. Unfavourable influences of nutrition on the factors of risk (hyperlipoproteinaemia, disturbance of the carbohydrate tolerance, hyperuricaemia, hyperalimentation) and on the manifest diseases (hypertension, diabetes mellitus, uric arthritis, obesity) of the metabolic syndrome which finally contribute to the development of arteriosclerosis are emphasized. In front of this background a clinically and ambulatorily tested basic metabolic diet is described. About 20% of the energy content (kcal or kJ) of this diet are protein, 35% fat and 45% are carbohydrates. The saturated fatty acids lie below 30%, the manifold saturated fatty acids, however, above 20% of the total fat proportion. The cholesterol content is below 400 mg, the purin-nitrogen below 200 mg, and the sodium content is about 2g per day. This diet can be produced for the treatment of persons with normal weight and overweight in different energetic degradations.
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PMID:[Nutrition and arteriosclerosis]. 70

The diagnostics of hyperlipoproteinaemias is essentially based on the proof of biochemical parameters. The simultaneous determination of triglycerides and cholesterol in the serum is the most important measure for establishing disturbances of the lipid metabolism. The behaviour of these two lipids, the consideration of the serum and the lipoprotein electrophoresis in most cases make possible a classification according to the distributed all over the world and clinically relevant division according to Fredrickson. Loading tests for the early recognition of hyperlipoproteinaemias - analogus to protodiabetes - are hitherto not yet known. Within the diagnostics shoude be taken into consideration that hyperliproproteinaemias are frequently associated with other metabolic diseases (obesity, gout, diabetes mellitus, hypertension) as so-called metabolic syndrome.
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PMID:[Diagnosis of primary hyperlipoproteinemias]. 90 91

It is well known that excessive weight is associated with resistance to insulin-mediated glucose uptake and predisposition to the development of type II diabetes. It has been shown more recently that excessive weight and insulin resistance tend to be associated to android fat distribution, arterial hypertension, elevated levels of triglycerides, low concentration of HDL cholesterol and defective fibrinolysis. The terms syndrome of insulin resistance, metabolic syndrome or syndrome X have been proposed to describe this cluster of abnormalities. The pathophysiological mechanisms which could explain the interrelations between these different parameters are still only partly understood. Epidemiological prospective studies have demonstrated that the metabolic syndrome is a risk factor for coronary heart disease and type II diabetes. The mechanisms involved in the development of diabetes are relatively well established, but those which are implicated in the atherothrombotic process are far from being clearly described. Anyway, sufficient presumption exists to attempt at decreasing insulin resistance when it exists. Physical training and, if indicated, weight reduction are the simplest means.
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PMID:The syndrome of insulin resistance. 130 11

Abdominal obesity is closely associated with risk factors for cardiocerebrovascular disease and NIDDM and the precipitation of these diseases. Together, they seem to constitute a metabolic syndrome where hyperinsulinaemia, insulin resistance, hyperlipidaemia, hypertension, visceral fat accumulation, cardiocerebrovascular disease and NIDDM are the individual constituents. The background to this syndrome might be a primary aberration expressing itself as an increased sensitivity of the hypothalamo-adrenal axis, and subsequent inhibition of sex steroid hormone secretions. This in turn will probably be followed by metabolic derangements, primarily peripheral insulin resistance, as well as by visceral fat accumulation by mechanisms which are partially visualized by recent work in the field. Visceral fat accumulation may then amplify the metabolic aberrations via hepatic effects of excessive concentrations of portal FFA, producing hyperproteinaemia, hyperglycaemia, hyperinsulinaemia and, perhaps, hypertension. The background to the central endocrine aberration remains more speculative, but factors leading to increased cortisol production, including specific stress reactions, tobacco smoking and alcohol may turn out to be important. The tentative conclusion provides a hypothesis for further work, and has recently obtained considerable support from further observations in humans in other than the endocrine and metabolic areas, as well as from studies in experimental animal models, where such factors can be studied under fully controlled conditions, which is not possible in humans for ethical reasons.
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PMID:Regional fat distribution--implications for type II diabetes. 133 83

Hypertension has previously been suggested to be a part of a metabolic syndrome also involving hyperlipidemia, hyperinsulinemia, and decreased insulin sensitivity. In the present study, 10 untreated hypertensive subjects were challenged with a high-salt diet (20 g NaCl) for 1 week after 7 days on a low-salt diet (less than 3 g). The difference in mean blood pressure (MBP) at the end of the high-salt diet v the low-salt diet was denoted salt sensitivity. We related the salt sensitivity to indices of glucose and lipid metabolism and studied the effect of salt deprivation on these metabolic variables. Salt sensitivity was found to be significantly correlated to HDL cholesterol (r = 0.79, P less than .007), insulin sensitivity (M value at the euglycemic clamp, r = 0.68, P less than .003), and fasting serum insulin (r = 0.69, P less than .04). Salt deprivation induced an increase in fasting insulin (P less than .03), but did not significantly affect any other indices of glucose and lipid metabolism. In conclusion, our study shows that hyperinsulinemia, decreased sensitivity to insulin, and low levels of HDL cholesterol were most commonly seen in hypertensive subjects with a low sodium sensitivity. A putative mechanism might be an increased activity in pressor systems also affecting glucose and lipid metabolism.
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PMID:Metabolic cardiovascular risk factors and sodium sensitivity in hypertensive subjects. 138 59

A clustering of metabolic disturbances has been indicated in hypertension. The distribution of such factors was assessed among hypertensives and normotensives in a general population sample of 644 men aged 67 years. Fasting serum insulin, glucose and triglyceride levels were measured. In this study hypertension was defined as DBP > or = 95 mmHg or present use of antihypertensives. Impaired glucose tolerance (IGT) or diabetes mellitus, hyperinsulinaemia (> or = 20 mU l-1) and hypertriglyceridaemia (> or = 2.3 mmol l-1) were defined as metabolic disturbances. When all these disturbances were present simultaneously a complete 'metabolic syndrome' was considered to be present. Hypertension was found in 185 (29%) men, IGT in 15%, diabetes mellitus in 11%, hyperinsulinaemia in 18% and hypertriglyceridaemia in 19%. Among hypertensives, 11 (6%) men had a 'metabolic syndrome', compared to 12 (3%) men in the normotensive group (P = 0.039). At least one metabolic disturbance was present in 109 (59%) of the hypertensive men, and in 173 (38%) of the normotensive men (P < 0.001). The prevalence rates of metabolic disturbances did not differ significantly between lean (BMI < 26 kg m-2) and obese (BMI > or = 26 kg m-2) hypertensives. Only hypertriglyceridaemia was more frequent in obese than in lean hypertensives (20% vs. 37%, P = 0.015). The 'metabolic syndrome' was found in 6% of all hypertensives, which was twice as common as in the normotensive population. The 'metabolic syndrome' was uncommon in both lean and obese hypertensives (5% vs. 7%, NS). These findings indicate that hypertension and metabolic disturbances may have a common underlying cause, at least in some individuals.
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PMID:Metabolic disturbances in hypertension: results from the population study 'men born in 1913'. 145 22

Today, essential hypertension is considered to be genetically closely related to disordered peripheral glucose metabolism, and this situation is described by the term metabolic syndrome. Both diseases--hypertension and type II diabetes--submit the heart and arterial vessels to an unphysiological, chronic stress, which they can compensate only for a certain time. Today, when antihypertensive treatment is indicated, drugs capable of preventing late vascular injury while at the same time having the potency to reverse already existing organic changes, are employed. ACE-inhibitors are presently considered to be the most potent substances that are capable of exerting a positive effect on hypertension-associated changes, while not increasing the individual risk profile in the development of arteriosclerosis. The present paper discusses the new ACE-inhibitor, cilazapril, which can be administered in a practical single dose and develops a profile of action typical of ACE-inhibitors in hypertensives with and without an accompanying metabolic syndrome.
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PMID:[ACE inhibition with cilazapril. Major therapeutic aspects: hypertension and metabolic syndrome]. 147

The metabolic syndrome (syndrome X) is characterised by an association of elevated insulin levels, a tendency to obesity of the android type, a disturbance of lipid metabolism with elevated triglyceride levels and commonly associated hypertension. The underlying common cause of this syndrome appears to be insulin resistance of the skeletal muscles, which is related in particular to the non-oxidative glucose utilization on the part of the muscle. The molecular cause of this syndrome has not been clarified, but a defect in the signal transduction chain between the insulin receptor and glycogen synthase is suspected. Epidemiological studies have shown that the metabolic syndrome may be considered a preliminary stage of manifest type II diabetes. In addition, it appears to play a major role in the development of cardiovascular complications in certain high-risk groups.
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PMID:[Pathophysiologic principles of metabolic syndrome. Consequences for early diagnosis and prevention]. 148 14

Essential hypertension in patients with the metabolic syndrome is regularly associated with other metabolic disorders. Thus, most hypertensives are overweight and have a glucose intolerance, while many have concomitant hyperproteinemia and dyslipoproteinemia. Up until fairly recently, it was not known that so-called insulin resistance is a common denominator both of metabolic risk factors and hypertension. In recent years, our knowledge about insulin resistance has spawned an equally convincing and fascinating multidimensional concept which reveals and plausibly explains complex relationships between metabolism, hypertension and the coronary risk.
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PMID:[Hypertension in metabolic syndrome. Etiology and consequences]. 148 16

Epidemiological studies have documented the association between cardiovascular disease and high blood pressure, dyslipidaemia, impaired glucose tolerance, non-insulin-dependent diabetes mellitus (NIDDM), and central obesity. In fact, several of these abnormalities, often all of them, can be identified in the very same individuals, constituting the entity of the multiple metabolic syndrome. Furthermore, many of these abnormalities seem to run in families. These findings raise important questions about the genetic epidemiology of the disease and about the molecular genetic background of the most likely common nominator of this syndrome, namely insulin resistance. Therapeutic actions must also be carefully considered to avoid the encouragement of some abnormalities while treating others.
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PMID:Multiple metabolic syndrome: aspects of genetic epidemiology and molecular genetics. 148 39


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