The metabolic syndrome is a constellation of metabolic and vascular abnormalities that include insulin resistance with compensatory hyperinsulinemia, central or visceral obesity, hypertension, dyslipidemia, microalbuminuria, and oxidative stress as well as prothrombotic and inflammatory abnormalities that contribute to a hypercoagulable state and systemic endothelial dysfunction. Visceral adipose tissue is now known to secrete into the circulation a number of protein and nonprotein factors that regulate glucose metabolism in traditional insulin-sensitive tissue as well as nontraditional insulin-sensitive tissue including cardiovascular tissue. Collectively, this constellation of factors that lead to metabolic dysregulation contributes to a substantial risk for adverse cardiovascular and renal outcomes. The development of a particularly resistant form of hypertension in these individuals can be attributed to a number of factors including vasoconstriction from increased sympathetic activation, proinflammatory cytokines, and inappropriate activation of the renin-angiotensin-aldosterone system. The management of hypertension in such patients can be challenging and generally requires nonpharmacologic as well as pharmacologic interventions.