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

Hypertension appears to predispose to both atheroma and thrombus formation and is a risk factor for stroke and coronary artery disease. Insulin resistance and hyperinsulinaemia are also associated with hypertension, whether treated or untreated and irrespective of obesity. In an attempt to treat the possible insulin resistance in hypertension, an antidiabetic agent, metformin, which enhances glucose uptake, was given to non-obese, non-diabetic, untreated hypertensives in a pilot study. Metformin improved insulin sensitivity, decreased plasma insulin, serum cholesterol and triglycerides, increased fibrinolytic activity and markedly decreased blood pressure. These findings support the concept that insulin resistance may be important in cases of primary hypertension, i.e. those with concomitant metabolic and possibly also fibrinolytic abnormalities. Furthermore, the results indicate that insulin resistance may precede hypertension in these cases.
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PMID:Metformin and blood pressure. 158 82

Insulin resistance associated with hyperinsulinemia (metabolic syndrome) emerged in recent years as an important health risk which is present in approximately 25% of the normal population in western industrialized societies. Insulin resistance as assessed for the whole body arises from a reduced glucose utilization of skeletal muscle. If the metabolic syndrome persists over a prolonged period of time, detrimental influences on the cardiovascular system become apparent involving diabetes mellitus, hypertension, and arteriosclerosis. Of particular pathogenic relevance is an unbalanced influence of insulin arising either from a diminished or enhanced insulin action depending on whether the various tissues of the body exhibit a reduced or unchanged insulin sensitivity. Since insulin resistance and hyperinsulinemia appear to be affected by various lifestyle factors, the unique opportunity exists of reducing cardiovascular mortality by correcting this syndrome at a time when degenerative changes have not occurred in the cardiovascular system. Of great importance is the finding that dietary factors can have a modulatory action on insulin sensitivity. In animal experiments, an increased intake of (saturated) fat and refined carbohydrates increased insulin resistance. Since psychosocial distress is expected to be associated with a sustained activation of the sympathoadrenal axis, it is likely also to aggravate the metabolic syndrome. A factor with a beneficial action appears to be physical exercise. In view of the high incidence of cardiovascular diseases, further research on lifestyle factors with an insulin-sensitizing or insulin-desensitizing action is required. Of prime importance is the reevaluation of established dietary recommendations and diets should be designed which take into account the individual cardiovascular risk factor profile.
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PMID:Insulin resistance, hyperinsulinemia, and cardiovascular disease. The need for novel dietary prevention strategies. 159 Jul 42

To determine if structural changes in forearm resistance vessels are associated with insulin resistance, we evaluated the relation between minimum forearm vascular resistance and insulin resistance in 95 obese adolescents before and after weight loss. Insulin resistance was assessed by fasting insulin levels and sum of insulin values after an oral glucose tolerance test in all 95 subjects and whole body glucose uptake during euglycemic hyperinsulinemia in 35 of 95 subjects. Structural changes in forearm vessels were assessed by measurement of minimum forearm vascular resistance during 10 minutes of ischemic exercise. As compared with our normal values, obese adolescents had a significantly (p less than 0.01) decreased maximal forearm blood flow (41.6 +/- 1.4 versus 67.1 +/- 2.4 ml/min/100 ml) and increased minimum forearm vascular resistance (2.9 +/- 0.4 versus 1.6 +/- 0.7 mm Hg/ml/min/100 ml). There was a significant relation (p less than 0.01) between minimum forearm vascular resistance and fasting insulin, sum of insulins, and whole body glucose uptake. After a 20-week weight-loss program, minimum forearm vascular resistance decreased (3.0 +/- 0.3 versus 2.0 +/- 0.2, p less than 0.01), maximal forearm blood flow increased (41 +/- 2.3 versus 57.4 +/- 3.9, p less than 0.01), and forearm volume remained unchanged. We also observed a significant (p less than 0.01) relation between the decrease in minimum forearm vascular resistance and the decrease in fasting insulin (r = 0.29), decrease in sum of insulins (r = 0.42), and increase in whole body glucose uptake (r = 0.63).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Forearm resistance vessel abnormalities and insulin resistance in obese adolescents. 159 57

Hypertension is only one component of a multifaceted metabolic-hemodynamic complex that also includes obesity, subtle and overt glucose intolerance, dyslipidemia, enhanced vascular resistance and accelerated atherosclerosis. Results of a number of studies in the past 5 years have shown that even nonobese, nondiabetic individuals with hypertension display insulin resistance, which is located in peripheral tissues (primarily skeletal muscle), is limited to nonoxidative pathways of glucose disposal, and appears to be directly correlated with the severity of hypertension. Insulin resistance and associated hyperinsulinemia in hypertensive individuals are also associated with increased plasma triglyceride levels and decreased high-density lipoprotein concentrations, which likely contributes to enhanced atherosclerosis. Hyperinsulinemia may directly promote atherosclerosis by enhancing LDL-cholesterol accumulation in vessel walls, vascular smooth muscle migration, and proliferation, augmenting connective tissue synthesis in the vascular wall, and decreasing the regression of lipid plaques. The enhanced peripheral vascular resistance that characterizes insulin resistance/hyperinsulinemic states may be related to decreased vascular smooth muscle responses to insulin, which normally modulates (attenuates) vascular contractile responses to vasoactive agents.
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PMID:Insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and accelerated atherosclerosis. 163 39

Plasma glucose and insulin responses to an oral glucose challenge and fasting plasma lipid and lipoprotein concentration were compared in 25 normal individuals and 53 patients with high blood pressure. Patients with hypertension were further subdivided into two groups--normal electrocardiogram (EKG) (n = 24) or abnormal EKG (n = 29)--using the Minnesota code criteria. Patients with hypertension and an abnormal EKG had significantly higher plasma glucose and insulin concentrations following oral glucose than did the control population. Furthermore, plasma triglyceride (TG) concentration was higher and high density lipoprotein cholesterol concentration lower then normal in hypertensive patients with an abnormal EKG, and the ratio of total to HDL cholesterol was higher in this subgroup. Values for patients with high blood pressure and a normal EKG were intermediate. Insulin-mediated glucose uptake was also measured in a subset of patients with hypertension and either a normal (n = 18) or abnormal (n = 17) EKG. When these two subgroups were compared, those with high blood pressure and an abnormal EKG were significantly more insulin resistant than patients with hypertension and a normal EKG. In addition, they also had higher plasma glucose and insulin responses to oral glucose, higher fasting plasma triglyceride and cholesterol concentrations, and an increase in the ratio of total to HDL cholesterol. Thus, patients with high blood pressure have abnormalities of glucose, insulin, and lipid metabolism when compared to a nonhypertensive control group, and the magnitude of these metabolic defects is significantly greater in patients with high blood pressure who have EKG evidence of coronary heart disease.
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PMID:Insulin resistance and abnormal electrocardiograms in patients with high blood pressure. 163 16

This study examines the relation between sympathetic activity and in vivo insulin-mediated glucose metabolism in a rat model of acquired hypertension. Two groups of conscious, unrestrained rats were studied in the postabsorptive state: sham-operated normotensive rats (n = 10) and renal-wrapped hypertensive rats (n = 10). Mean arterial pressure was increased in the hypertensive compared with the normotensive group in the fed (184 +/- 9 versus 144 +/- 6 mm Hg; p less than 0.01) and in the fasting (147 +/- 8 versus 112 +/- 7 mm Hg; p less than 0.01) state. After a 24-hour fast, hepatic glucose production, plasma glucose, insulin, and norepinephrine concentrations were similar in the two groups. Blood pressure did not change in either group during the 3-milliunits/kg.min euglycemic insulin clamp study; however, plasma norepinephrine concentration rose significantly in hypertensive (207 +/- 24 versus 329 +/- 11 pg/ml; p less than 0.05) but not in normotensive rats (229 +/- 23 versus 267 +/- 27 pg/ml; p = NS). During the insulin clamp study, the hepatic glucose production was similar in the hypertensive (3.8 +/- 0.8 mg/kg.min) compared with the normotensive (4.0 +/- 0.3 mg/kg.min) rats. Insulin-mediated glucose uptake was significantly higher in hypertensive than in normotensive rats (33.0 +/- 0.7 versus 25.8 +/- 0.8; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Aug
PMID:Increased insulin sensitivity in the high sodium one-kidney, one figure-8 hypertensive rat. 163 60

Insulin resistance associated with a hyperinsulinemic response to oral glucose intake has been found in patients with essential hypertension and is believed to play a role in inducing hypertension by causing renal sodium and water retention. We therefore examined whether salt-sensitive, young normotensives, assumed to be predisposed to essential hypertension, exhibit impaired glucose tolerance in a similar way. The plasma insulin and glucose response to oral glucose intake (75 g) was assessed in 23 healthy, lean, male volunteers ingesting either 20 mmol or 260 mmol NaCl/day for 6 days each in a single-blind randomized crossover study. Salt sensitivity was defined as a significant drop in mean arterial blood pressure greater than 3 mmHg (means of 30 readings in the supine subject; P less than 0.05) under the low-salt diet. Following the glucose load, plasma levels of both glucose and insulin were significantly higher (P less than 0.01) in the salt-sensitive (n = 10) compared with the salt-resistant subjects (n = 13) during the high-salt diet but not during the low-salt diet. Whereas in the salt-sensitive group glucose tolerance improved with dietary salt restriction (P less than 0.01), it deteriorated in the salt-resistant group (P less than 0.05). Following the glucose load under the high-salt diet, there was a significant drop in blood pressure in the salt-sensitive (P less than 0.005) but not the salt-resistant subjects. The hyperglycemic and hyperinsulinemic response in salt-sensitive subjects suggests that insulin resistance is present in these subjects prior to the development of hypertension and that it can be ameliorated by salt restriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Salt sensitivity in young normotensive subjects is associated with a hyperinsulinemic response to oral glucose. 164 59

When Australian Aborigines make the transition from their traditional hunter-gatherer life-style to a westernized life-style, they develop high prevalence rates of obesity (with an android pattern of fat distribution), non-insulin-dependent diabetes, impaired glucose tolerance, hypertriglyceridemia, hypertension, and hyperinsulinemia. Insulin resistance may be the common pathogenetic characteristic of this cluster of conditions associated with increased risk of cardiovascular disease. The traditional hunter-gatherer life-style, characterized by high physical activity and a diet of low energy density (low, fat, high fiber), promoted the maintenance of a very lean body weight and minimized insulin resistance. In contrast, for most Aborigines, western life-style is characterized by reduced physical activity and an energy-dense diet (high in refined carbohydrate and fat) that promotes obesity and maximizes insulin resistance. Intervention strategies aimed at prevention of insulin-resistance-related chronic disease should be directed at life-style modification. To be effective, such programs will have to be developed and controlled by Aboriginal communities.
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PMID:Westernization and non-insulin-dependent diabetes in Australian Aborigines. 166 99

The effects of insulin on Na(+)-H+ exchange were examined in isolated proximal segments from normotensive Sprague-Dawley (SD) and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with monitoring of rates of intracellular pH change (delta pHi/min) and ethylisopropyl amiloride (EIPA)-suppressible 22Na+ uptakes. A 12-min insulin preincubation was necessary for steady-state 22Na+ uptake and rate of pHi change. Insulin responses were similar for 4-wk (prehypertensive) SHR and WKY tubules; 8- (rising hypertension) and 16-wk (established hypertension) SHR responses were increased (P less than 0.05) 23 and 36% with 10(-6) M insulin, respectively. Insulin-like growth factors (IGF-I, IGF-II; 10(-10)-10(-7) M) had no effect on Na(+)-H+ exchange activity. Incubation with physiological concentrations of insulin in combination with hormones that stimulate Na(+)-H+ exchange (angiotensin II; alpha-adrenoceptor agonists) demonstrated no synergistic increases in SHR or WKY tubules; incubation with hormones that inhibit Na(+)-H+ exchange [parathyroid hormone (PTH), dopamine (DA)] indicated that insulin stimulation was decreased with PTH or DA in WKY segments, but PTH or DA reduction of insulin stimulation was lacking in SHR tubules. In summary, these data indicate a direct stimulation by insulin of Na(+)-H+ exchange in the proximal nephron, indicate an increased responsiveness in SHR compared with WKY tubules, and suggest a modulatory role of insulin with other hormones in regulating proximal nephron Na(+)-H+ exchange.
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PMID:Insulin increases Na(+)-H+ exchange activity in proximal tubules from normotensive and hypertensive rats. 167 43

Essential hypertension and non-insulin-dependent diabetes mellitus are both associated with hyperinsulinemia and it has been proposed that this might contribute to increased atherogenesis in these conditions. In hypertension, hyperinsulinemia probably reflects reduced insulin-stimulated glucose uptake, but the reason for this, and the contribution of hyperinsulinemia (or of resistance to insulin) to the development of hypertension and atheroma, remains unclear. As well as glucose uptake, insulin has important effects on other aspects of cell function; for example, the hormone is an important regulator of the expression and function of the major inhibitory guanine nucleotide binding protein Gi. In insulin deficiency, Gi levels and function are greatly reduced and are restored by insulin treatment. We have examined whether in human hypertension or in animal models of hypertension there is evidence of abnormal regulation of this protein. Platelet membranes from humans and rat membranes from a range of tissues, including myocardium and vasculature, were studied. No alteration in Gi levels or function was found in these studies, and there is no evidence that this aspect of insulin action on cell function is abnormal. Insulin is also involved in the regulation of cell growth, and in vascular smooth muscle cells there is evidence that this effect involves action of other growth factors, such as PDGF. If the growth regulatory actions of insulin are also unimpaired despite limitation of insulin-stimulated glucose uptake, chronic hyperinsulinemia could lead to increased vascular smooth muscle cell growth and contribute to development of atheroma.
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PMID:Hypertension, insulin, and atherogenesis. 172 42


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