Hypertension is often accompanied by a host of metabolic defects. Investigations have shown an association between insulin resistance, hyperinsulinemia, central/visceral obesity, and hypertension. Recent interest has focused on the fact that untreated hypertensive individuals have compensatory hyperinsulinemia, are resistant to insulin-mediated glucose uptake, and frequently have coexisting lipid abnormalities. Data from prospective studies appear to indicate that fasting hyperinsulinemia is an independent predictor of coronary artery disease. Additionally, there is evidence that hyperinsulinemia and diabetes eliminate the normal sex differences in the prevalence of coronary artery disease. The salutary effects of ovarian hormones on the prevalence of hypertension and cardiovascular disease in postmenopausal women are well established. Hyperandrogenism, in particular elevated serum levels of dehydroepiandrosterone sulfate, is believed to be a risk factor promoting sex-specific impairments of glucose and lipid metabolism, obesity, and hypertension in women. Clinical and epidemiologic evidence have linked elevated blood pressure to disturbances in lipoprotein metabolism, fibrinolytic activity, plasminogen activation inhibitor levels, and dyslipidemia. This review briefly presents the current understanding of various metabolic disturbances associated with hypertension, the pathophysiologic mechanisms involved, and the significance of the interplay between them relative to the complications of this disease.