Reaven Gerald M.Journal of Cardiovascular Pharmacology: 1990 Original Article: PDF Only Free Abstract Patients with untreated hypertension have been shown to be resistant to insulin-stimulated glucose uptake. They are also hyperinsulinemic and hypertriglyceridemic when compared with matched control groups with normal blood pressure. In addition, insulin resistance, hyperinsulinemia, and hypertriglyceridemia have been demonstrated in rat models of hypertension, including spontaneous hypertensive rats and Sprague-Dawley rats led a fructose-enriched diet. The defect in insulin-stimulated glucose uptake in these experimental models can also be shown at the cellular level. Furthermore, experimental interventions that prevent insulin resistance or hyperinsulinemia from developing in fructose-fed rats also greatly attenuate increases in blood pressure. Endogenous hyperinsulinemia and hypertriglyceridemia have been identified as factors that increase the risk of coronary artery disease (CAD), and they may contribute to the increased prevalence of ischemic heart disease in patients with high blood pressure. The fact that past antihypertensive treatment has not focused on these metabolic abnormalities, and indeed may have exacerbated them, could help explain why it has been difficult to show that lowering blood pressure decreases the risk of CAD. These observations raise the possibility that abnormalities of carbohydrate and lipoprotein metabolism may play a role in both the etiology and the clinical course of hypertension. Copyright © 1990 Wolters Kluwer Health, Inc. All rights reserved.