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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance, hyperinsulinemia, and dyslipidemia are common characteristics of patients with untreated hypertension. However, the link between the vascular and metabolic disturbances is still unclear. To provide further insights into the metabolic picture of subjects with hypertension, we evaluated insulin resistance, pancreatic secretion, and hepatic extraction of the hormone in 16 untreated patients with essential hypertension before and after 12-16 weeks of drug treatment in comparison with 16 age-, sex-, and body weight-matched normotensive control subjects. All subjects underwent an oral and a frequently sampled intravenous glucose tolerance test. Metabolic parameters were calculated by the minimal model technique. The hypertensive patients exhibited a highly reduced tissue insulin sensitivity (2.6 +/- 0.4 versus 9.6 +/- 1.9 10(4) min-1/[microunits/mL]; p < 0.001). The basal secretion rate (70 +/- 11 versus 35 +/- 5 pmol/L per minute) and the total amount of prehepatically secreted insulin (32 +/- 4 versus 16 +/- 2 nmol/L in 4 hours) were significantly increased in the hypertensive patients compared with the control subjects (p < 0.01), whereas the posthepatic insulin delivery rate was not significantly different between the two groups (4.9 +/- 0.6 versus 3.5 +/- 0.3 nmol/L in 4 hours). Hepatic insulin extraction was found to be significantly elevated in the hypertensive patients compared with control subjects (81 +/- 4% versus 69 +/- 3%, p < 0.04). Increased hepatic insulin extraction partially ameliorated B cell hypersecretion in hypertensive patients. After 12-16 weeks of drug treatment, the blood pressure was normalized, but the metabolic profile of the patients remained unchanged. We conclude that elevated insulin extraction in the liver is a specific characteristic of individuals with essential hypertension and partially compensates pancreatic B cell hypersecretion.
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PMID:Elevated hepatic insulin extraction in essential hypertension. 849 99

GENETIC PREDISPOSITION: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean, young offspring, as well as in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension together with dyslipidemia, obesity and type 2 diabetes in a given patient. INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. Among the mosaic of assumed pressor mechanisms, distinct Na+ retention is almost invariably involved in diabetes mellitus, while sympathetic activation tends to occur in essential hypertension, particularly in association with obesity. Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or a decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or excess body weight. Acute hyperinsulinemia causes arterial vasodilation on one hand and increases sympathetic activity and renal Na+ reabsorption on the other. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, while insulin resistance may be associated with certain transmembraneous cation transporters, leading to an increase in cytosolic Ca2+. Hyperinsulinemia and/or insulin resistance may also be associated with an increased blood pressure sensitivity to high salt intake. In the mosaic of many different blood pressure-raising mechanisms, insulin resistance and/or hyperinsulinemia is likely to represent an amplifying slow or very slow pressor factor.
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PMID:Insulin resistance and hyperinsulinemia in hypertension. 857 90

The insulin resistance syndrome has been noted as an interesting and important new risk factor for coronary artery disease. The syndrome consists of hypertension, glucose intolerance, and dyslipidemia, all of which are likely to be derived from insulin insensitivity. In subjects with nonobese and nondiabetic essential hypertension, steady-state plasma glucose (SSPG) was higher than in normotensive subjects during an insulin sensitivity test, indicating reduced insulin sensitivity to glucose metabolism in the hypertensive group. SSPG correlated with the percentage decrease of branched chain amino acids, free fatty acids, and serum potassium during the insulin sensitivity test. With a 2-h insulin infusion, serum norepinephrine, epinephrine, plasminogen activator inhibitor 1, and intraplatelet Ca2+ decreased significantly, but 6-keto-prostaglandin (PG) F1 alpha and PGE2 did not change. Insulin resistance decreased by using antihypertensive treatments with bunazosin, cilazapril, amlodipine, and benidipine in hypertensive subjects. Diagnostic criteria for the insulin resistance syndrome, including clinical values for each risk factor, were developed. Lowered insulin sensitivity and hyperinsulinemia were demonstrated in subjects with both vasospastic and coronary artery stenotic angina. The insulin resistance syndrome together with hyperinsulinemia is likely to induce atherosclerotic changes, possibly through reduced rather than excessive action of insulin.
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PMID:Mechanism and clinical implication of insulin resistance syndrome. 867 91

Hypertension is not solely a phenomenon of elevation of systemic blood pressure. It frequently occurs in association with a great deal of metabolic derangement's and should never be regarded as coincidental only. Furthermore, a knowledge of these metabolic derangements may provide a clue to unveil the underlying mechanisms how essential hypertension and its associated complications arise. Therefore we devoted our attention to platelet dysfunction and dyslipidemia which are closely associated with atherosclerosis-the commonest complication of hypertension. We found there exists enhanced platelet aggregation in essential hypertension and a variety of its associated atherosclerotic diseases. Such an aberration in platelet function may be modified after administration of antihypertensive medications such as angiotensin converting enzyme (ACE) inhibitors, calcium channel blockades, beta blockades and dietary manipulation. We also demonstrated the close association between hypertension and its associated atherosclerotic complications and abnormal lipids profile. Hypertriglyceridemia which was initially regarded unimportant in the pathogenesis of atherosclerosis is found to be closely related to hypertension. In an intensive review, we found that people in Taiwan has experienced a huge increase in dietary calories and total fat consumption. In order to solve this emerging problem, a national guideline for diagnosis and management of lipid disorders in Taiwan was developed and announced. Through these efforts, we hope we can reduce the cardiovascular morbidity and mortality in Taiwan and even extend our experience to other countries.
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PMID:Thrombogenic and lipid risk factors in hypertension and coronary artery disease. 868 58

Data concerning hyperinsulinemia/insulin resistance in the pathogenesis of essential hypertension are presented. Approximately 50% of hypertensive patients have insulin resistance. The prime site of insulin resistance is in the skeletal muscle affecting non oxidative glucose metabolism (glycogen synthesis). Effects of insulin on the kidney points toward possible, but not the key role of the hyperinsulinemia in the pathogenesis of arterial hypertension. According to some results hypertension causes hyperinsulinemia/insulin resistance through hemodynamic alterations and structural changes of blood vessels. On the other hand, there is no hyperinsulinemia in the secondary forms of arterial hypertension. This is an argument against hypertension as a prime cause in insulin resistance inception. The importance of metabolic alterations of lipid status and fibrinolytic system in patients with hyperinsulinemia has been emphasized. These metabolic changes increase cardiovascular risk. Effects of antihypertensive drugs on glucose metabolism and insulin sensitivity are reported. In conclusion, hyperinsulinemia per se is not a risk factor. However, when connected with other metabolic disturbances (dyslipidemia, hypertension, hyperuricemia, disorders of fibrinolysis) it increases the risk of cardiovascular diseases.
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PMID:[Hyperinsulinemia and arterial hypertension]. 875 12

It has been reported that insulin resistance is associated with essential hypertension and that an aggregation of risk factors-hypertension, dyslipidemia, and glucose intolerance-together with insulin resistance leads to the more frequent appearance of coronary artery disease. We examined the relation between early asymptomatic atherosclerosis and these risk factors in 72 nondiabetic subjects with essential hypertension (41 men, 31 women) aged 50 to 59 years. Intima-media thickness and plaque formation of the carotid artery were assessed by B-mode ultrasonography, and insulin sensitivity was measured by the steady-state plasma glucose method. Lipoprotein profile was analyzed by ultracentrifugation. The intima-media thickness of the common carotid artery significantly correlated with systolic pressure; mean blood pressure; steady-state plasma glucose, indicating insulin resistance; fasting insulin; area under the curve of plasma insulin and glucose; body mass index; apolipoprotein B; apolipoprotein B in low-density lipoprotein; lower ratio of cholesterol to apolipoprotein B of low-density lipoprotein; and decreased high-density lipoprotein cholesterol. By multiple regression analysis, steady-state plasma glucose was the strongest risk, followed by lower high-density lipoprotein and systolic pressure. These three factors accounted for 54.9% of all the risk for increased intima-media thickness of the common carotid artery. In conclusion, insulin resistance was the strongest risk factor for carotid intima-media thickness, followed by lower high-density lipoprotein cholesterol and hypertension. An effort to maintain normal insulin sensitivity is essential for the prevention of early atheromatous lesions in essential hypertension.
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PMID:Insulin resistance as an independent risk factor for carotid wall thickening. 884 83

In an open, multicenter study, the calcium antagonist lacidipine was tested for efficacy and safety, particularly with respect to any influence on lipid and carbohydrate metabolism. The study was performed in 2,127 patients with essential hypertension. The patients were treated orally, with lacidipine in a dosage of 2-6 mg once daily for 48 weeks. Lacidipine significantly reduced both systolic and diastolic blood pressure by 20 +/- 17 mm Hg and 14 +/- 10 mm Hg, respectively, from baseline values (both p < 0.0001). Decreases in blood pressure were achieved without any adverse effects on lipid and carbohydrate metabolism, either in the total group or in subsets of diabetic or hyperlipidemic patients. It is concluded that lacidipine is a safe and effective drug in the long-term antihypertensive treatment of patients with essential hypertension and with concomitant metabolic disorders such as diabetes mellitus or dyslipidemia.
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PMID:The impact of lacidipine, a novel dihydropyridine calcium antagonist, on carbohydrate and lipid metabolism. 885 41

In normal subjects, insulin decreases the urinary excretion of sodium, potassium, and uric acid. We tested whether these renal effects of insulin are altered in insulin resistant hypertension. In 37 patients with essential hypertension, we measured the changes in urinary excretion of sodium, potassium, and uric acid in response to physiological euglycemic hyperinsulinemia (by using the insulin clamp technique at an insulin infusion rate of 6 pmol/min/kg). Glucose disposal rate averaged 26.6 +/- 1.5 mumol/min/kg, i.e., 20% lower than in normotensive controls (33.1 +/- 2.1 mumol/min/kg, P = .015) In the basal state, fasting plasma uric acid concentrations were higher in men than women (P < .001), were positively related to body mass index (r = 0.38, P = .02), waist/hip ratio (r = 0.35, P < .05), and serum triglyceride levels (r = 0.59, P = .0001), and negatively related to HDL cholesterol concentrations (r = -0.59, P = .0001) and glucose disposal rate (r = 0.42, P < .01). Uric acid clearance, on the other hand, was inversely related to body mass index (r = 0.41, P = .01), plasma uric acid (r = 0.65, P < .0001) and triglyceride concentrations (r = 0.39, P < .02), and directly related to HDL cholesterol levels (r = 0.52, P < .001). During insulin infusion, blood pressure, plasma uric acid and sodium concentration, and creatinine clearance did not change. In contrast, hyperinsulinemia caused a significant decrease in the urinary excretion of uric acid (2.67 +/- 0.12 to 1.86 +/- .14 mumol/min/1.73 m2, P = .0001), sodium (184 +/- 12 to 137 +/- 14 mumol/min/1.73 m2, P = .0001), and potassium (81 +/- 7 to 48 +/- 4 mumol/ min/1.73 m2, P = .0001). Both in absolute terms (clearance and fractional excretion rates) and percentagewise, these changes were similar to those found in normotensive subjects. Insulin-induced changes in urate excretion were coupled (r = 0.55, P < .0001) to the respective changes in sodium excretion. In hypertensive patients, higher uric acid levels and lower renal urate clearance rates cluster with insulin resistance and dyslipidemia. Despite insulin resistance of glucose metabolism, acute physiological hyperinsulinemia causes normal antinatriuresis, antikaliuresis, and antiuricosuria in these patients.
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PMID:Effect of insulin on renal sodium and uric acid handling in essential hypertension. 886 20

The spontaneously hypertensive rat (SHR) is the most widely used animal model of human essential hypertension. In the SHR strain, as in humans, the high blood pressure is determined multifactorially. Analysis of genetically segregating populations, derived from SHR and normotensive inbred strains, enabled localization of quantitative trait loci (QTLs) responsible for blood pressure regulation on several rat chromosomes. Analysis of specialized strains, congenic and recombinant inbred (RI) strains, helped to analyze some of these mapping results in detail: (1) analysis of congenic strains provided definitive evidence for the presence of blood pressure regulatory genes on chromosomes 8 and 13 and will enable mapping of responsible genes to limited segments of differential chromosomes, (2) the RI strains were shown to be especially useful for genome scanning studies of complex traits and for correlation analysis of blood pressure and other risk factors of cardiovascular disease such as cardiac hypertrophy, dyslipidemia, and insulin resistance.
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PMID:Recombinant inbred and congenic strains for mapping of genes that are responsible for spontaneous hypertension and other risk factors of cardiovascular disease. 899 35

It has been suggested that hyperinsulinemia secondary to insulin resistance may be a pathogenetic factor common to obesity, non-insulin-dependent diabetes mellitus (NIDDM), and hypertension. Furthermore, beta-blockers and thiazide diuretics have been shown to be capable of increasing insulin resistance and thus of inducing NIDDM in predisposed individuals. We used the minimal model approach (MMA) to glucose metabolism and insulin kinetics to compare peripheral insulin sensitivity and beta-cell function in hypertensive and normotensive obese men. The hypertensive group consisted of 37 obese men with mild to moderate hypertension; following a drug-free period of 4 weeks, 20 of these subjects received diltiazem and 17 quinapril over the 12-week study period. The normotensive (control) group contained 17 obese men without microalbuminuria, dyslipidemia, or a family history of essential hypertension or NIDDM. Before and at the end of the 12-week study period, subjects underwent frequently sampled intravenous glucose tolerance (FSIGT) tests. The results were used to estimate an insulin sensitivity index (S(I)), a glucose effectiveness index (S(G)), and beta-cell sensitivity to glucose indices during first- and second-phase insulin secretion (phi1 and phi2) using the minimal models of glucose metabolism and insulin kinetics. No significant differences in S(I) or S(G) were detected between the hypertensive and control groups. Twelve weeks' treatment with diltiazem led to a slight but significant increase in phi1; however, neither diltiazem nor quinapril had significant effects on S(I) or S(G). We conclude that men with obesity and hypertension have no greater insulin resistance than those with obesity alone, suggesting that hypertension is not generally associated with any significant increase in insulin resistance. Treatment with diltiazem or quinapril does not have undesirable effects on glucose metabolism. However, treatment with diltiazem led to a significant increase in beta-cell sensitivity to glucose; this is of particular interest, given the importance of phi1 for peripheral glucose uptake.
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PMID:Insulin sensitivity, glucose effectiveness, and beta-cell function in obese males with essential hypertension: investigation of the effects of treatment with a calcium channel blocker (diltiazem) or an angiotensin-converting enzyme inhibitor (quinapril). 903 Aug 25


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