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

Aging is associated with an increased incidence of hypertension, noninsulin-dependent diabetes mellitus, and coronary heart disease. Because these conditions often cluster in the same individuals, there has been speculation that a common mechanism is responsible for all of these pathological states. Both epidemiological and clinical research has shown that insulin resistance and/or hyperinsulinemia are associated with glucose intolerance, dyslipidemia (high plasma triglyceride and low high-density lipoprotein-cholesterol levels), and higher systolic and diastolic blood pressures. Therefore, insulin resistance and hyperinsulinemia have been proposed as the causal link among the elements of the cluster mentioned above, now most commonly referred to as the insulin resistance syndrome, syndrome X, or the metabolic syndrome. The elderly are more glucose intolerant and insulin-resistant, but it remains controversial whether this decrease in function is an inevitable consequence of "biological aging" or the result of what might be referred to as environmental or lifestyle variables: increased obesity, a detrimental pattern of fat distribution, or physical inactivity that usually accompany age. All of these modifiable environmental factors have also been shown to result in increases in insulin resistance and hyperinsulinemia and are risk factors for the development of the diseases of the metabolic syndrome. Recent interventional studies that have attempted to reverse these conditions in the elderly have shown improved insulin sensitivity, and glucose tolerance. Insulin secretion, on the other hand, seems to decrease with age even after adjustments for differences in adiposity, fat distribution, and physical activity. This may be responsible for the glucose intolerance in the very old even after improvements have been made in their lifestyle variables.
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PMID:The effect of age on insulin resistance and secretion: a review. 882 67

Rather than a link in a causal chain leading to hypertension, insulin resistance and resultant hyperinsulinemia may be 'spokes on a wheel', with central or visceral obesity as the postulated hub of the wheel. Hypertension, hypertriglyceridemia and high density lipoprotein cholesterol are depicted as other spokes. Newly identified metabolic pathways in adipose tissue or the modulating effects of various predisposing genes may lead to variable expression of various components of the multiple metabolic syndrome in individuals with a predisposition to the collection of visceral fat.
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PMID:Hypertension, dyslipidemia, and insulin resistance: links in a chain or spokes on a wheel? 888

One of the characteristics of peripheral vascular disease in diabetic patients is that it occurs at the time of detection of diabetes mellitus. As one of the possible pathogenic mechanisms, in non-smokers, is the sol-called metabolic syndrome (obesity, disorders in regard to metabolism of lipids and carbohydrates and hypertension). Lipoprotein Lp(a) is the most atherogenic among lipoproteins. While data on coronary arterial disease exist, although contradictory, there is a small number of those which document the same for peripheral vascular occlusive disease in diabetics. Two patients, non-smokers, with characteristic constellation of risk factors, are described as possible models for further epidemiologic examinations.
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PMID:[The metabolic syndrome and hyper-Lp(a)-lipoproteinemia in peripheral obliterative atherosclerosis: 2 case reports]. 892 51

Considerable progress has been made in our understanding of the role of the nervous system in human hypertension. The evidence for a widespread autonomic abnormality in the early phases of hypertension is overwhelming and excessive sympathetic activity is consistently present in such patients since their childhood. The enhanced sympathetic tone in hypertension is associated with the metabolic syndrome of insulin resistance and dyslipidemia. Multiple mechanisms by which sympathetic overactivity could cause both hypertension and the metabolic syndrome have been documented. Furthermore, the excessive sympathetic tone is conducive to coronary heart disease through its association with high hematocrit values and with excessive platelet aggregability. Surprisingly, the myth that patients with neurogenic hypertension have a benign prognosis continues to persist. Much of the misunderstanding stems from the idea that patients with neurogenic hypertension, commonly called "white coat" or borderline hypertension, do not develop established hypertension. There is no support for such an assessment; in fact, patients with neurogenic hypertension are at a high risk of future accelerated hypertension. Another misunderstanding relates to differences in hemodynamics between neurogenic and established hypertension. It is true that patients with neurogenic hypertension initially show an increase of cardiac output. However, this later evolves into a classic picture of established high resistance hypertension. The hemodynamic transition is secondary to a decrease in cardiac responsiveness and an increase in vascular responsiveness over the course of hypertension. With passage of time, vascular reactivity increases, yet sympathetic tone tends to decrease. This can be explained by the "blood pressure seeking behavior of the central nervous system." In hypertension, the central nervous system appears to seek a higher blood pressure level and, as the vasculature becomes hyperresponsive, less sympathetic tone is needed to maintain the elevated blood pressure. This decrease of sympathetic tone in later phases of hypertension should not be viewed as a normalization, since sympathetic tone in relationship to vascular hyperresponsiveness remains excessive and the central nervous system maintains a crucial role in sustaining high blood pressure in hypertension.
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PMID:Sympathetic overactivity in hypertension. A moving target. 893 44

Hypertension is associated with metabolic disturbances that may be related to hyperinsulinemia, both resulting from our lifestyle. Insulin resistance generated by central obesity, and complex relations with sympathetic activity, dyslipemia, atherosclerosis, sodium retention, altered vascular reactivity and hypertension, lead to pathophysiological connections, that are still to be understood. Even if obesity and hypertension were not related through hyperinsulinemia, the metabolic syndrome increases either vascular risk or hypertension, and it has to be re-evaluated whether essential hypertension is an adequate diagnosis for these patients.
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PMID:[Metabolic syndrome with vascular risk and arterial hypertension]. 893 72

Recently, an inverse correlation between serum uric acid concentrations and insulin sensitivity has been described in subjects with varying degrees of metabolic syndrome, suggesting that measurement of serum uric acid may provide a simple marker of insulin resistance. Several biochemical and clinical features of polycystic ovary syndrome (PCOS) resemble those of metabolic syndrome: women with PCOS are often obese; they are also at increased risk for the development of coronary artery disease, hypertension and diabetes mellitus. The objective of the present study was to analyse the usefulness of serum uric acid measurement in screening for the metabolic syndrome in women with PCOS. For that purpose serum concentrations of uric acid, insulin and triglycerides were measured in 38 women with PCOS and 20 weight-matched control women with regular menstrual cycles. No differences were found in the uric acid concentrations between the PCOS and control groups. The mean concentrations of triglycerides and fasting insulin were higher in the women with PCOS than in the healthy controls. Serum uric acid concentrations were inversely related to serum hormone-binding globulin (SHBG) concentrations, and positively with body mass index (BMI), insulin concentrations and testosterone:SHBG ratio in the PCOS group. Our results suggest that measurement of serum uric acid does not provide new means for identification of metabolic syndrome in patients with PCOS.
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PMID:Normal serum uric acid concentrations in women with polycystic ovary syndrome. 898 Nov 20

A group of metabolic disorders including insulin resistance and hyperinsulinemia, impaired glucose tolerance, visceral obesity, hypertension, dyslipidemia, hyperuricemia, hypercoagulability and microalbuminuria determine the risk for the development of atherosclerosis, coronary artery disease and cerebral vascular disorders. Although available studies on the pathogenesis of the metabolic syndrome are equivocal, it is most frequently hypothesized that hereditary of insulin resistance leads to the remaining metabolic disorders including diabetes mellitus, atherosclerosis and coronary artery disease. Despite pathogenetic controversies, there are convincing arguments for the diagnosis of the metabolic syndrome and search for therapy improving insulin sensitivity and reducing hyperinsulinemia thus preventing the development of diabetes mellitus and coronary artery disease.
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PMID:[Insulin resistance and hyperinsulinemia--clinical aspects]. 899 30

Croatian Endocrine Society and Croatian Academy of Medical Sciences organized Symposium on Hyperandrogenaemia on March 22nd, 1996. Different aspects of this syndrome were discussed: epidemiology, classification and clinical features, steroid biosynthesis in the adrenal gland and ovarium, the genetics of polycystic ovarian syndrome (PCOS), clinical significance of testosterone and dihydrotestosterone metabolism, androgen excess and metabolic syndrome (syndrome X), insulin disturbances in PCOS, increased risk for development of non insulin dependent diabetes mellitus, androgen effects on serum lipoproteins, insulin like growth factors and function of ovarium, Doppler parameters in PCOS, treatment of hyperandrogenaemia, skin changes in PCOS, tests for adrenal and ovarial function, arterial hypertension and hyperinsulinism. National Board of Hyperandrogenaemia has been elected.
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PMID:[National consensus on hyperandrogenemia]. 901 36

Metabolic syndrome is characterized by a large number of metabolic disorders, the findings being generally a combination of insulin resistance, obesity, hypertension, dislipidemia and pathological glucose tolerance or diabetes mellitus type II. Metabolic syndrome is diagnosed too seldom in view of the fact that a prevalence of at least 10% must be assumed for the population as a whole. Besides genetic predisposition, environmental factors such as diet, physical inactivity and nicotine and alcohol consumption play a decisive role in its clinical manifestation. The paper briefly examines the pathophysiological connections between the individual findings, with the central role of insulin resistance being emphasized. With a multifactorial therapy, in which non-medicamentous treatment is predominant, it must be assumed that on the whole compliance will tend to be poor. Prognostically the syndrome is serious, very frequently resulting in premature atherosclerosis. The paper concludes with a consideration of the underwriting of metabolic syndrome, one of the points being that the extramortality rates of the individual impairments should not be applied additively.
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PMID:[Prognostic aspects of metabolic syndrome. Is the "good living" syndrome regarded seriously enough in general insurance medicine practice?]. 901 97

Noninsulin-dependent diabetes mellitus is a genetically determined form of diabetes, due to impaired insulin secretion by the B-cells as well as to insulin resistance of the peripheral tissues. According to the glucose toxicity theory hyperglycemia and hyperinsulinemia exist in a vicious circle. Therefore, it is a major therapeutical aim to put the B-cell to rest and improve insulin sensitivity by a strict control of fasting blood glucose and of postprandial hyperglycemia. Furthermore, associated abnormalities within the metabolic syndrome, such as hypertension, dyslipoproteinemia and hemostatic disorders should be corrected to avoid vessel complications. Therefore, it should be started with basic measures as body weight reduction, carbohydrate-rich and fat-poor diet and exercise. If these measures fail to achieve acceptable glycemic control, antihyperglycemic drugs (acarbose, metformin) are indicated, eventually in a combination with small doses of short-acting sulfonylureas. Further impairment of insulin secretion is the indication for sulfonylurea and/or insulin application. HbA1c of 7 to 7.5% should be the goal of antidiabetic therapy, also for patients in advanced age. The main criterion for the choice of antidiabetics is the present insulin secretion capacity. Simple indicators in this respect are changes of body weight, plasma triglycerides and C-Peptide after i.v. glucagon stimulation. Application of insulin in combination with other antidiabetics or in the form of intensified insulin therapy should not be too much postponed.
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PMID:[Rational therapy of Type II diabetes]. 903 69


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