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(Hypertension. 1996;28:219-223.)
© 1996 American Heart Association, Inc.
Articles |
Attenuation of Hypertension by Insulin-Sensitizing Agents
Correspondence to Theodore A. Kotchen, MD, Department of Medicine, Medical College of Wisconsin, 9200 W Wisconsin Ave, Milwaukee, WI 53226.
Key Words: insulin resistance • hyperinsulinism • insulin
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Introduction |
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Epidemiological and clinical evidence document an association between hypertension and resistance to insulin-stimulated glucose uptake.1 Insulin-resistant individuals also tend to have increased plasma concentrations of triglycerides and low-density lipoprotein cholesterol and decreased concentrations of high-density lipoprotein cholesterol. These associations have been observed in individuals with type II diabetes and in obese people. In addition, depending on methodologies and criteria for its definition, insulin resistance is present in 16% to 40% of nonobese individuals with essential hypertension and in normotensive individuals who are at increased risk for developing hypertension.1 2 Insulin resistance may be associated with salt sensitivity of blood pressure.3 4 5
Insulin resistance has also been observed in both genetic and acquired rat models of hypertension, eg, the Dahl salt-sensitive (Dahl S) rat, spontaneously hypertensive rat (SHR), Milan hypertensive rat, and rats with sucrose or fructose feeding.1 However, insulin-stimulated glucose uptake is normal in both the one-kidney, one clip hypertensive rat and the two-kidney, one clip hypertensive rat, suggesting that insulin resistance is not an invariable consequence of elevated arterial pressure.6 7
Although a number of putative mechanisms have been proposed, it is unclear whether insulin resistance and/or hyperinsulinemia actually cause hypertension.1 Insulin itself is a vasodilator, and in normal subjects, insulin infusions along with sufficient glucose to prevent hypoglycemia cause vasodilation, not vasoconstriction.8 Individuals with insulinoma do not have an increased prevalence of hypertension,9 although in this situation hyperinsulinemia is primary and is not due to insulin resistance.
In a variety of circumstances, increasing insulin sensitivity and/or reversal of hyperinsulinemia is associated
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