Over the past century, uric acid has been considered a possible risk factor for hypertension and cardiovascular disease. However, only in the past decade, animal models and clinical trials have supported a more mechanistic link. Results from animal models suggest a 2-phase mechanism for the development of hyperuricemic hypertension in which uric acid induces acute vasoconstriction by activation of renin-angiotensin system, followed by uric acid uptake into vascular smooth muscle cells leading to cellular proliferation and secondary arteriolosclerosis that impairs pressure natriuresis. This acute hypertension remains uric acid dependent and sodium independent, whereas the chronic hypertension becomes uric acid independent and sodium dependent. Small clinical trials, performed in adolescents with newly diagnosed essential hypertension, demonstrate that reduction of serum uric acid can reduce blood pressure. Although more research is clearly necessary, the available data suggest that uric acid is likely causative in some cases of early onset hypertension.