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Ferrannini Eleuterio; Haffner, Steven M.; Stern, Michael P.
Journal of Cardiovascular Pharmacology: 1990
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Epidemiological evidence supports a link between hyperinsulinemia and blood pressure. In nondiabetic. normotensive individuals, the male sex, age, obesity, and body fat distribution all arc 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, nondi-abetic 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. In conclusion, (a) hyperinsulinemia and insulin resistance are consistently associated with hypertension independently of obesity and NIDDM; (b) the insulin resistance of essential hypertension manifests itself mostly as a selective inability of insulin to stimulate glycogen synthesis in skeletal muscle: and (c) although probably under genetic control, insulin resistance is insufficient to explain the prevalence of hypertension against a divergent ethnic background.

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