Patients with untreated hypertension have been shown to be resistant to insulin-stimulated glucose uptake and both hyperinsulinemic and hypertriglyceridemic when compared to matched control groups with normal blood pressure. All of these abnormalities would be accentuated in obese individuals. In addition, insulin resistance, hyperinsulinemia, and hypertriglyceridemia have been demonstrated in rat models of hypertension, including rats with spontaneous hypertension and Sprague-Dawley rats fed a fructose-enriched diet, and 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 and/or hyperinsulinemia from developing in fructose-fed rats also greatly attenuate the increase in blood pressure. Since endogenous hyperinsulinemia and hypertriglyceridemia have been identified as factors that increase the risk of coronary artery disease, it is likely that they 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 risk of coronary artery disease. 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.