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

A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension. Hyperinsulinemia has been recognized as a major risk factor for the development of coronary artery disease independent of blood pressure and plasma lipid levels. All these conditions are frequently associated, particularly in aging, a state itself characterized by hyperinsulinemia. This common association has prompted the hypothesis that hyperinsulinemia may be a causative factor rather than the consequence of obesity, diabetes, hypertension, and hyperlipidemia. If that is the case, defining the nature and mechanisms of hyperinsulinemia becomes of primary interest. Insulin resistance is also a striking feature of all of the above mentioned pathologic states. In the presence of a preserved B-cell function, hyperinsulinemia can represent the mechanism designed to overcome the defect in the biological action of the hormone. For instance, there is a clear-cut age-related decline in the body's sensitivity to insulin. In order to compensate for this defect in insulin-mediated glucose metabolism, the B-cell must increase its secretion. On the other hand, a certain degree of insulin resistance can be induced both in animals and man by prolonged euglycemic hyperinsulinemia. Little is known regarding possible primary defects of the B-cell leading to uncontrolled oversecretion of insulin and subsequent insulin resistance. The primary defect, more probably, resides in an alteration of one or more of the steps whereby insulin exerts it own action. In favor of this hypothesis are the observations that insulin resistance segregates in familial clusters and that the first defect found in normoglycemic relatives of insulin-resistant diabetic patients is a reduced transformation of glucose into glycogen. Whatever is the primary defect, it is likely that a correction of insulin resistance might reduce the circulating levels of plasma insulin, possibly playing a beneficial effect on glucose tolerance, body weight, blood pressure and plasma lipid concentration.
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PMID:[Hyperinsulinism. Causes and mechanisms]. 133 21

The combined syndrome of android (upper body) obesity, diabetes, hyperlipidaemia and hypertension is discussed in terms of a deranged endocrine regulation of metabolism. The syndrome is characterized by insulin insensitivity and an increased control of metabolism by cortisol. The antagonism between the two hormones appears to be partly responsible for the hyperglycaemia, hypertriglyceridaemia and hypercholesterolaemia. The synergism between insulin and cortisol in stimulating energy deposition, associated with a decreased effect of corticotropin-releasing factor in stimulating energy expenditure, is likely to contribute to the development of obesity. The efficacy of D-fenfluramine in treating the obese-diabetic-hyperlipidaemic-hypertensive syndrome probably depends on its actions on the serotoninergic system in the hypothalamus which both decreases food consumption and tends to normalize hormonal balance through the hypothalamic-pituitary-adrenal axis.
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PMID:Neuroendocrine regulation and obesity. 133 26

Current treatment of obesity seems to be focused mainly on the success of losing body weight, which can be achieved, in order of increasingly drastic manoeuvres: by simple nutritional advice; professional follow-up of a negative energy balance; drugs with effects on appetite regulation, energy absorption or expenditure; total seclusion with control of every administered calorie; surgical intervention; or even jaw-wiring. The only treatment of this sort that has been convincingly shown to have long-lasting effects is surgical intervention in the gastrointestinal tract, but this can only be accepted for use in severe cases. Thus, the problem of treatment of moderate obesity is to find an effective therapeutic modality which iss efficient in maintaining a reduced weight. Obesity treatment also seems to have focused too much on the mass of excess body fat, which is not necessarily an indicator of the medical hazards of the condition. It is important to realize that the risk factor clusters following obesity are often efficiently treated by successful reduction of the obese condition. Instead of specific treatment of each of these complications by, for example, multi-pharmacological therapy, a sufficiently efficient obesity treatment would be a preferable substitute. This goal may, if necessary, be achieved by treatment with a single drug with a useful therapeutic profile, including efficiency in the long-term to prevent relapse. Chronic treatment might then be considered acceptable in the same way as chronic pharmacological treatment of hypertension and hyperlipidemia, for example. No drug has as yet proven to have these characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of obesity. 133 27

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

To assess the factors which may initiate and accelerate degenerative senile calcification of the aortic valve, two-dimensional echocardiograms and the clinical characteristics of 259 consecutive cases with senile calcification of the aortic valve were studied. The results were compared with those of similar studies among 186 consecutive cases with the normal aortic valves. An aortic cusp with an area of increased echo greater than 3 mm in width and with decreased pliability was regarded as calcified. Among patients with calcification of one aortic cusp, 114 exhibited calcification of a noncoronary cusp, 17 calcification of the left coronary cusp and 3 calcification of the right coronary cusp (p < 0.001). Among patients with calcification of 2 aortic cusps, 39 had calcification of a noncoronary and left coronary cusps, 3 calcification of the left and right coronary cusps and 16 calcification of the right and noncoronary cusps (p < 0.001). In patients with calcification of their aortic valves, the end-diastolic angle between the interventricular septum and the ascending aorta was 102 +/- 10 degrees; whereas, it was 89 +/- 10 degrees in the control group (p < 0.001). There were no differences in frequency of aortic root calcification, mitral annular calcification, hypertension, ischemic heart disease, hyperlipidemia, hyperuricemia, or hyperglycemia, between patients with and without calcification of their aortic valves. Of the female patients ranging in age from 65 to 74 years, 88% in those with calcification of 3 cusps and 30% in those with calcification of one cusp (p < 0.05) had mitral annular calcification.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Influence of systolic left ventricular blood flow direction on genesis of senile calcification of the aortic valve]. 133 4

In the 1970s in the Diet-Antismoking Trial, of the Oslo Study, colleagues and I found that the majority of high-risk men with elevated serum cholesterol and elevated triglyceride concentrations had impaired fibrinolytic capacity. Later on, both our group and others found a similar negative correlation between serum triglyceride levels and fibrinolytic capacity. Furthermore, in a prospective study of dietary intervention in individuals with both elevated cholesterol and triglyceride levels, we found that dietary lowering of serum triglyceride levels was significantly and positively correlated with an improvement in fibrinolytic capacity. In another study, we made the same observation for the coagulation factor VII-phospholipid complex: the more the triglycerides were reduced by diet, the greater was the change in factor VII complex. This correlation was highly significant and independent of changes in serum cholesterol. Platelet function is also influenced by dietary habits, but except for the effects of a fish oil-enriched diet, few data are available about the dietary effects on platelet function. It seems, however, that in individuals with elevated lipid levels and elevated blood pressure, increased platelet reactivity is a highly prevalent finding. Many of the hemostatic risk variables are associated with the so-called "metabolic risk syndrome" characterized by an increase in serum insulin level, together with increased relative body weight, mild hypertension, hyperlipidemia, and physical inactivity. This syndrome can often be influenced favorably by life-style changes. A controlled study with interventions in diet and activity level has just been started by our group.
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PMID:The influence of dietary change on hemostatic risk variables. 134 3

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.
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PMID:Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit. 138 26

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

This study was designed to assess the effect of hyperlipidemia on cardiovascular responses to adrenergic stimulation in a porcine model. Four-week-old piglets (n = 10) were divided into two groups; one fed a control diet and the other was fed an atherogenic diet for 8 weeks. Cardiovascular responses were evaluated to both norepinephrine (NE; 0.5 and 2.5 micrograms/kg) and isoproterenol (ISO; 0.1 and 0.5 microgram/kg) from simultaneous recordings of femoral arterial pressure, heart rate, left intraventricular pressure and left intraventricular dP/dt. It was found that no significant difference in the baseline values of cardiovascular function was observed between the control and hyperlipidemic groups. However, in the hyperlipidemic group as compared with the control group: 1) arterial blood pressure responses to NE were significantly increased (P less than 0.05), 2) cardiac contractile responses to NE and ISO were significantly potentiated (P less than 0.05), and 3) reflex bradycardia in response to increasing arterial blood pressure did not occur. These findings indicate that hyperlipidemia can potentiate the cardiovascular responses to adrenergic stimulation, whereas reflex cardiovascular regulation is somewhat altered by hyperlipidemia. Conceivably, these observations may have relevance to the possible role of the mechanism of the interaction of hyperlipidemia and hypertension in atherogenesis.
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PMID:Effect of hyperlipidemia on cardiovascular responses to adrenergic stimulation in piglets. 139 Nov 72

This paper sums up the clinical epidemiological investigation data on risk factors (RF) of coronary heart disease (CHD) among 743 office workers, with an average age of 61.0 +/- 8.0. The investigation involved factors relating to history, physical examination, biochemistry, blood rheology and TCM Syndrome Differentiation. According to the results of the computerized single-factor correlation analysis, the incidence of CHD in RF exposed group was obviously higher than that of unexposed one, 65 RF such as hypertension, diabetes, hyperlipemia, smoking, body weight, HDL-C/TC, blood viscosity etc. were recorded. Using multivariate regressive analysis it revealed that hypertension, diabetes, total cholesterol, heavy cigarette smoking, overweight, diastolic pressure, cortisol, TCM senile index, Blood Stasis Syndrome, Qi Stagnation Syndrome, Qi Deficiency Syndrome and Heart Deficiency Syndrome were the main RF. The result concerning RF of Western medicine (WM) was in conformity with that at home and abroad. In addition, some TCM-RF were selected which couldn't be replaced by WM-RF. These indicate that there are TCM-RF and WM-RF in the development of CHD and it is better to adopt the method for preventing and treating CHD with combined TCM-WM. As to TCM-RF of CHD, the authors consider that there are both the factors of Deficiency and Excess, so preventing and treating CHD should aim at reinforcing the Deficiency and reducing the Excess.
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PMID:[Clinical epidemiological study on risk factors of coronary heart disease in 743 subjects]. 139 88


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