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

Non-insulin-dependent diabetes (NIDDM) has long been recognized as being associated with a cluster of disorders including obesity, hypertension, dyslipidemia, and atherosclerotic heart disease. It was only recently, however, that Reaven, DeFronzo, and Ferrannini with techniques to quantitate insulin resistance suggested that this represents a common factor in this group of disorders and that hyperinsulinemia resulting from insulin resistance could be the cause of the hypertension, dyslipidemia, and atherosclerosis. The names syndrome X or the insulin-resistance syndrome have been used to identify this pathological entity, and considerable investigations have been done and are in progress to establish whether or not these coexisting disorders represent an as yet unexplained association of cardiovascular risk factors or if, indeed, insulin resistance and hyperinsulinism represent the primary cause for most of the other disorders. To paraphrase a philosophical comment, if syndrome X did not exist, we probably would have had to invent it. In addition to the intellectual satisfaction of being able to "lump" these diverse ills under a single etiology, the main value of grouping these disorders as a syndrome is to continually remind physicians that the therapeutic goals are not only to correct hyperglycemia in NIDDM but also to manage the elevated blood pressure and dyslipidemia that cause cerebrovascular and cardiac morbidity as well as mortality in these patients. Having a syndrome X reduces the fragmentation of medical care among subspecialties and decreases the likelihood of prescribing drugs that correct hypertension but raise lipids or drugs that lower lipids but raise blood glucose. Finally, it encourages the selection of drugs that reduce hyperglycemia without increasing insulin secretion and to the development of new drugs for this purpose. Unfortunately, the concept of insulin resistance with hyperinsulinism being a cause of the other associated disorders is still unproved but continues to be open to experimental investigation. The remainder of this article reviewed the use of sulfonylureas in the management of NIDDM, discussed new molecular and cellular mechanisms by which they promote insulin secretion, and reviewed the controversy as to whether an extrapancreatic action contributes to their glucose-lowering effects in NIDDM. A closing section listed some other oral drugs that can lower blood glucose without stimulating the pancreatic beta cell. Their insulin-sparing hypoglycemic effect makes them potentially useful in NIDDM therapy, particularly if the fundamental premise of syndrome X is substantiated, which implicates hyperinsulinemia as contributing to the morbidity and mortality from atherosclerotic vascular disease.
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PMID:Type II diabetes and syndrome X. Pathogenesis and glycemic management. 161 69

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

The objective of treating patients with hypertension is not simply to reduce blood pressure but rather to prevent the associated morbidity and mortality. Recent assessments of clinical trials have shown that while the risk of stroke is consistently lower with antihypertensive therapy, the same degree of success has not been demonstrated for coronary artery disease (CAD). Although there are many explanations of why we have not done as well in preventing CAD, one possibility is that the therapy used in clinical trials, primarily thiazide diuretics and beta-adrenoreceptor blockers, has increased the patient's risk of developing coronary atherosclerosis or lethal arrhythmias. Four classes of antihypertensive agents are recommended for initial therapy--thiazide diuretics, beta-adrenoreceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium entry blockers. The metabolic effects of thiazide diuretics include electrolyte disturbances (hypokalemia, hypomagnesemia, and hyponatremia), dyslipidemia (increased triglycerides), abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance), and hyperuricemia. beta-Adrenoreceptor blockers have many of the same metabolic adverse reactions. beta-Adrenoreceptor blockers without intrinsic sympathomimetic activity (ISA) also cause dyslipidemias (lowered high-density lipoprotein cholesterol and increased triglycerides) and abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance). beta-Adrenoreceptor blockers with ISA and third-generation beta-blockers with selective partial agonist activity (celiprolol and dilevalol) do not cause dyslipidemia and to date do not appear to induce abnormalities in glucose metabolism. ACE inhibitors may decrease triglycerides and increase high-density lipoprotein cholesterol, and captopril may improve insulin sensitivity. Calcium entry blockers are metabolically neutral.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic considerations in the choice of therapy for the patient with hypertension. 167 Nov 90

Epidemiological evidence supports a link between hyperinsulinemia and blood pressure. In nondiabetic, normotensive individuals, the male sex, age, obesity, and body fat distribution all are associated with higher systolic and diastolic blood pressure and with higher plasma insulin concentrations. Nevertheless, when accounting for the above physiological variables, blood pressure still is independently related to plasma insulin. In the general population, hypertensive individuals have multiple metabolic abnormalities (glucose intolerance, hyperinsulinemia, and dyslipidemia). A striking pattern of overlap exists among obesity, diabetes, and hypertension. Physiological studies (euglycemic insulin clamp) have shown that essential hypertension per se is a state of insulin resistance: lean, nondiabetic subjects with untreated hypertension have a mean 40% reduction in the ability of physiological hyperinsulinemia to stimulate whole-body glucose uptake. Other insulin actions (suppression of hepatic glucose output, lipolysis, lipid oxidation, and promotion of K+ uptake) are conspicuously preserved. In perfused forearm studies, local (intra-arterial) hyperinsulinemia induces subnormal rates of glucose uptake and glycogen synthesis in the skeletal muscle of individuals with essential hypertension. In the San Antonio Heart Study, parental history of non-insulin-dependent diabetes mellitus (NIDDM) is associated with hyperinsulinemia and higher blood pressure and serum lipid levels in nondiabetic probands. In this biethnic population, however, hyperinsulinemia and NIDDM are more prevalent (approximately threefold) among Mexican-Americans than non-Hispanic whites, but hypertension is more prevalent among the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Essential hypertension: an insulin-resistant state. 169 27

Hypertension, dyslipidemia, and glucose intolerance cocluster in the population and act synergistically in increasing coronary artery disease risk. The mechanisms by which these risk factors interact in atherosclerosis are complex. First, hypertension, dyslipidemia, and altered insulin sensitivity may have a common pathophysiological basis. Activation of neurohormonal mechanisms may be implicated in many or all of these processes. In addition, underlying these processes may be common genetic and environmental influences. Second, these risk factors ultimately act on the blood vessel, thereby leading to atherosclerosis. Elevated serum lipids lead to vessel wall responses, including endothelial dysfunction, smooth muscle cell proliferation, lipid accumulation, foam cell formation, and, eventually, necrosis and plaque development. Hypertension may induce shear-related injury to the vessel. Endothelial injury (caused by hypertension) and vascular cell proliferation (induced by increased pressure and/or vasoactive substances) are effects that amplify the atherosclerotic process. In addition, diabetes and hyperinsulinemia can increase vascular tone, impair endothelial function, and stimulate vascular smooth muscle cell proliferation. Control of these risk factors should prevent or attenuate the vessel wall responses. Emphasis is now being placed on pharmacological therapeutic modalities that decrease blood pressure and improve insulin sensitivity and lipid metabolism. Identification of common links between risk factors, such as neurohormonal mechanisms (e.g., angiotensin), should lead to better therapeutic strategies.
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PMID:Atherosclerosis and hypertension: mechanisms and interrelationships. 169 33

Non-insulin-dependent (type II) diabetes mellitus is an inherited metabolic disorder characterized by hyperglycemia with resistance to ketosis. The onset is usually after age 40 years. Patients are variably symptomatic and frequently obese, hyperlipidemic and hypertensive. Clinical, pathological and biochemical evidence suggests that the disease is caused by a combined defect of insulin secretion and insulin resistance. Goals in the treatment of hyperglycemia, dyslipidemia and hypertension should be appropriate to the patient's age, the status of diabetic complications and the safety of the regimen. Nonpharmacologic management includes meal planning to achieve a suitable weight, such that carbohydrates supply 50% to 60% of the daily energy intake, with limitation of saturated fats, cholesterol and salt when indicated, and physical activity appropriate to the patient's age and cardiovascular status. Follow-up should include regular visits with the physician, access to diabetes education, self-monitoring of the blood or urine glucose level and laboratory-based measurement of the plasma levels of glucose and glycated hemoglobin. If unacceptably high plasma glucose levels (e.g., 8 mmol/L or more before meals) persist the use of orally given hypoglycemic agents (a sulfonylurea agent or metformin or both) is indicated. Temporary insulin therapy may be needed during intercurrent illness, surgery or pregnancy. Long-term insulin therapy is recommended in patients with continuing symptoms or hyperglycemia despite treatment with diet modification and orally given hypoglycemic agents. The risk of pancreatitis may be reduced by treating severe hypertriglyceridemia (fasting serum level greater than 10 mmol/L) and atherosclerotic disease through dietary and, if necessary, pharmacologic management of dyslipidemia. Antihypertensive agents are available that have fewer adverse metabolic effects than thiazides and beta-adrenergic receptor blockers. New drugs are being developed that will enhance effective insulin secretion and action and inhibit the progress of complications.
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PMID:Non-insulin-dependent (type II) diabetes mellitus. 174 94

The rise of arterial pressure in elderly and senile persons reflects morphological alterations in the vessels, the development of sympathetic hyperactivation and adrenoreceptor dysfunction rather than can be referred to compensatory and adaptation reactions of the body. The treatment of patients suffering from arterial hypertension should be aimed at preventing the development of fibrinoid arterial necrosis which may occur because of regular antihypertensive therapy and dyslipidemia correction.
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PMID:[Arterial hypertension and its treatment in the aged]. 175 7

Overall 183 children with arterial hypertension (AH) were examined. Of these, 122 suffered from primary arterial hypertension (PAH). The lipid spectrum was defined in blood plasma of 95 children with PAH and in 30 normals. The same investigation was carried out in 109 parents of the children suffering from PAH. The lipid spectrum was established to be heterogeneous. 77.9% of the patients had dyslipidemia. A significant relationship was established between the stage of PAH and the nature of lipidemia as was a close interrelation between alterations in the lipid spectrum of blood plasma and hereditary load as regards essential hypertension.
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PMID:[The characteristics of lipid metabolism in children with primary arterial hypertension]. 176 67

Cardiovascular disease, and in particular ischemic heart disease, is the principal cause of morbidity, functional disability, and mortality in patients with non-insulin-dependent (type II) diabetes. The main risk factors for the macrovascular complications of diabetes are dyslipidemia, hypertension, and cigarette smoking. Although degree of hyperglycemia is a risk factor for microvascular complications, it is not a prominent risk factor for macrovascular complications. Nevertheless, there are theoretical reasons for believing that glycemic control could lower cardiovascular risk. For example, glycemic control may both improve clearance and suppress hepatic overproduction of very-low-density lipoprotein. Moreover, there is direct empirical evidence that improved glycemic control can favorably alter lipid profiles in type II diabetic patients. Despite this, the only clinical trial that has assessed cardiovascular mortality as an end point in diabetic subjects (i.e., the University Group Diabetes Program) failed to demonstrate a benefit of glycemic control. In this study, the insulin-variable group, which achieved sustained glycemic control relative to the placebo group, had essentially the same cardiovascular mortality as the latter group. All of the conventional lipid-lowering agents have been shown to produce favorable changes in lipid profiles in diabetic subjects. However, the optimum regimen remains to be defined. Metabolic differences between diabetic and nondiabetic subjects mean that the optimum lipid-lowering regimens for the two categories of patients may differ. For example, nicotinic acid, which is a powerful lipid-altering drug, may worsen glucose intolerance. The characteristic lipid abnormalities in type II diabetic subjects are hypertriglyceridemia and low high-density lipoprotein cholesterol, not hypercholesterolemia. Although the role of hypertriglyceridemia as a cardiovascular risk factor in the general population has been questioned, there is evidence that this lipid abnormality may play a stronger role in diabetic subjects. For all of the above reasons, there is an urgent need for large-scale clinical trials assessing cardiovascular end points and testing various strategies of improving lipid profiles in diabetic subjects, particularly given the fact that all of the current generation of lipid-lowering trials have systematically excluded diabetic patients.
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PMID:Dyslipidemia in type II diabetes. Implications for therapeutic intervention. 177 1

Hyperandrogenism and lipid metabolism were shown to be related intimately. Any discussion of the nature of their relationship must include other clinical and metabolic variables such as hyperinsulinemia and UBO. Despite the many correlations among each of these factors, the appropriate sequence in the pathogenesis of these conditions has not been defined. Do conditions that result in insulin resistance (e.g., genetic defects, insulin receptor antibodies, and obesity) also lead to the development of hyperandrogenemia by direct or indirect ovarian stimulation by insulin? Does hyperandrogenism of ovarian or adrenal origin cause abnormal upper body fat distribution, in turn leading to lipid abnormalities and insulin resistance? Regardless of the issue of mechanism of causality, women with hyperandrogenism are thought to be at greater risk for cardiovascular morbidity and mortality than their normoandrogenic counterparts. These women often are obese, hypertensive, and sedentary; ingest diets high in saturated fats; and have glucose intolerance and/or insulin resistance. All these abnormalities are well known independent risk factors for the development of lipid abnormalities and cardiovascular disease. Whether hyperandrogenism is a secondary consequence of any of these or whether it is an independent contributor to lipid aberrations requires future study. Treatment strategies for hyperandrogenic women, however, should not only be directed toward alleviation of the cosmetic problem of hirsutism but also toward the prevention and treatment of cardiovascular morbidity using modalities aimed at eradicating hyperinsulinemia, hypertension, and dyslipidemia. These modalities should include modifications in diet, exercise, and weight in addition to pharmacologic and/or surgical manipulation. Weight reduction will reduce many cardiovascular risk factors. Obesity is easier to target because of the many risk factors that result in it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipid metabolism and hyperandrogenism. 177 28


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