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Hyperinsulinemia and insulin resistance have been implicated to play a role in the development of hypertension and to contribute to the increased risk for cardiovascular disease in diabetic, obese, hypertensive, and normotensive salt-sensitive humans. Reviewed herein are the effects of nonpharmacological measures, including exercise, weight loss, diet, and changes in lifestyle, on insulin resistance. Based on the evidence from both experimental and clinical studies, regular exercise, moderate weight reduction, and a low-fat, high-carbohydrate, high-fiber diet can markedly improve insulin sensitivity. The possible mechanisms involved are discussed. Because these nonpharmacological measures have also been shown to lower blood pressure and correct dyslipidemia, they can contribute substantially to the reduction of major cardiovascular risk factors and should be implemented in all patients who may be at risk for cardiovascular disease.
J Cardiovasc Pharmacol 1992
PMID:Effects of nonpharmacological intervention on insulin sensitivity. 128 41

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
J Cardiovasc Pharmacol 1992
PMID:Hypertension and insulin resistance. 128 47

The major risk factors apply in the elderly as well as the young, including hypertension, dyslipidemia, impaired glucose tolerance, physical indolence, and [table: see text] cigarette smoking. These risk factors are highly prevalent in the elderly and are not inevitable consequences of aging and genetic makeup. With aging, there is a longer exposure to risk factors and diminished capacity to cope with them, resulting in a doubled incidence of cardiovascular sequelae at any level of risk factors compared with younger candidates for cardiovascular disease. The predisposing modifiable risk factors for coronary disease, stroke, cardiac failure, and peripheral arterial disease are virtually the same in younger and older candidates for cardiovascular disease. Multivariate cardiovascular risk profiles predict cardiovascular disease as efficiently in the elderly as in the young. There is also evidence that recurrent cardiovascular events are influenced by the same risk factors that predispose to initial events. Although proof of the efficacy of modifying risk factors in older persons is limited to hypertension control, recent declines in coronary and stroke mortality in the United States have included the elderly. This justifies extrapolations of data from the middle aged until sorely needed data become available on the efficacy of modifying risk factors in the elderly.
Cardiovasc Clin 1992
PMID:Epidemiology of cardiovascular disease in the elderly: an assessment of risk factors. 153 33

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)
J Cardiovasc Pharmacol 1990
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.
J Cardiovasc Pharmacol 1990
PMID:Atherosclerosis and hypertension: mechanisms and interrelationships. 169 33

Atherosclerosis and its various clinical manifestations are now highly predictable and preventable diseases. Dyslipidemia appears to be a necessary cause, and hypertension and cigarette smoking are both powerful and modifiable contributing causes. Health professionals should incorporate cardiovascular risk assessment and risk factor modification within the context of their delivery of personal health services. Such services probably already have contributed to the decline of cardiovascular mortality, and the current levels of risk factors in the United States population indicate that substantial further reduction should be possibly by creating a smoke-free environment by the year 2000 and by implementing the recommendations of the National Cholesterol and High Blood Pressure Education Programs.
Cardiovasc Clin 1990
PMID:Cardiovascular risk factors. 218 65

Essential hypertension is a heterogeneous group of disorders with different causes. This report reviews approaches taken and results found in current studies of the genetic and environmental determinants of essential hypertension. Recent observations from the University of Utah Cardiovascular Genetics Research Clinic and published data from other studies are cited. Several biochemical tests show strong associations with hypertension and substantial major gene and/or polygenic determination including: urinary kallikrein excretion, intracellular sodium concentration, sodium-lithium countertransport, plasma haptoglobin phenotypes, MN blood groups, and familial dyslipidemia.
J Cardiovasc Pharmacol 1988
PMID:Definition of genetic factors in hypertension: a search for major genes, polygenes, and homogeneous subtypes. 246 8

Several drugs used for antihypertensive therapy may modify the lipoprotein metabolism. Thiazides in high dosage and loop diuretics can increase serum low-density lipoprotein (LDL) cholesterol and/or very-LDL cholesterol and the total cholesterol/high-density lipoprotein (HDL) cholesterol ratio, while HDL cholesterol is largely unchanged; triglycerides (Tg) are also often elevated. Premenopausal women may be protected from this side effect. Whether diuretic-induced dyslipidemia is dose-dependent and low thiazide doses (i.e., hydrochlorothiazide < or = 12.5 mg daily) are interacting less, awaits clarification. beta-Blockers without intrinsic sympathomimetic activity increase serum triglycerides and tend to lower the potentially antiatherogenic HDL cholesterol. The diuretic-antihypertensive agent indapamide, given at a dose of 2.5 mg/day, is neutral with regard to serum lipoprotein and glucose metabolism. The potassium-sparing diuretic spironolactone, conventional sympatholytic agents, calcium-channel blockers, and probably the serotonin2-receptor antagonist ketanserin, exert no relevant effects on the lipoprotein profile. Angiotensin-converting enzyme inhibitors may slightly decrease serum triglycerides. alpha 1-Receptor blockers slightly decrease LDL cholesterol and Tg and increase HDL cholesterol. Drug-induced development or aggravation of dyslipidemia represents a potentially adverse influence. In the hypertensive population, effective blood pressure control with traditional drug therapy based on thiazide-type diuretics in high dosage led to a distinct decrease in cerebrovascular morbidity and mortality, but failed to satisfactorily reduce coronary complications. The prognostic relevance of drug-induced changes in serum lipoproteins, carbohydrate metabolism and other risk factors or correlates awaits further clarification.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1993
PMID:Serum lipoproteins during treatment with antihypertensive drugs. 750 69

Reviewed herein are data supporting the hypothesis that insulin and the sympathoadrenal system are involved in the pathogenesis of hypertension in the obese. Data from the Normative Aging Study, a population-based cohort followed in Boston, confirm other epidemiologic reports of a direct relationship between upper-body obesity, hyperinsulinemia, and hypertension. Because insulin is known to stimulate the sympathetic nervous system (SNS), the possibility that insulin-mediated sympathetic stimulation contributed to hypertension in the obese was investigated by the analysis of 24-h urinary norepinephrine (NE) excretion in this group. Urinary NE was directly correlated with body mass index and waist/hip ratio, supporting increased SNS activity in the obese. Epinephrine excretion, an index of adrenal medullary activity, was inversely related to obesity, and both high insulin and low epinephrine levels were independently correlated with lower levels of high-density lipoprotein cholesterol and higher levels of triglycerides. These results are consistent with the hypothesis that insulin-mediated sympathetic stimulation results in hypertension from concomitant sympathetic stimulation of the heart, vessels, and kidney. Reciprocal changes in adrenal medullary function contribute to the associated dyslipidemia. Therapeutic strategies aimed at diminishing insulin resistance and lowering insulin levels, and antagonizing the effects of sympathetic stimulation on the heart, the vessels, and the kidneys, would appear to have a solid physiological rationale in the obese.
J Cardiovasc Pharmacol 1994
PMID:Pathophysiology of obesity-related hypertension: role of insulin and the sympathetic nervous system. 751 90

So-called insulin resistance is a frequent phenomenon and a marker of increased risk for both type II diabetes mellitus and atherosclerosis. Today, insulin resistance is widely understood as a tissue- and pathway-specific defect of insulin-stimulated glucose uptake into skeletal muscle that is compensated for by hyperinsulinemia, leading to a cluster of undesirable hypertensiogenic, diabetogenic, and atherogenic processes. Additional defects of insulin-stimulated muscle blood flow and cellular kation balance are presently attracting increasing awareness. Clinical and experimental evidence suggests that angiotensin-converting enzyme (ACE) inhibition ameliorates both insulin-stimulated skeletal-muscle glucose uptake and blood flow in insulin-resistant states by a direct stimulation of cellular glucose uptake, which appears to be kinin-mediated. This improvement of insulin sensitivity could mean not only improvement of glucose metabolism, but also reduction of chronically elevated serum insulin and the ensuing atherogenic consequences (hyper- and dyslipidemia, sympathetic overactivity, growth of vascular smooth-muscle cells, hypertension, etc.). Ca(2+)-channel blockers that do not increase heart rate appear to exert direct antiatherogenic effects while being metabolically neutral. Thus, the combination of Ca(2+)-channel blockade by sustained release verapamil and ACE inhibition by trandolapril in insulin-resistant type II diabetic patients with essential hypertension appears to be promising in terms of possible synergistic effects.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1994
PMID:Possible synergistic effect of ACE inhibition and calcium-channel blockade on insulin sensitivity in insulin-resistant type II diabetic hypertensive patients. 751 94


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