 The investigators have reported a clear relationship between higher serum uric acid and increased intrarenal angiotensin II as assessed by intravenous angiotensin II Ang II infusions in human subjects.11 In this model, the change in renal blood flow in response to infused Ang II serves as an indirect indicator of renal vascular exposure to endogenous Ang II. In the setting of high endogenous intrarenal Ang II, renovascular AT1 receptors are down-regulated and the normal reduction in renal blood flow in response to infused exogenous Ang II becomes blunted. The investigators found that increased serum uric acid is strongly correlated to blunting of the normal response to infused Ang II. Other studies by our colleagues in Boston have demonstrated that treatment with ACE inhibitors or angiotensin receptor blockers restores normal responsiveness to infused Ang II in hypertensives with this blunted response and that such patients may be particularly responsive to RAS blockade.12-14 The studies in rats and our results with the association of uric acid suggest that elevated uric acid may cause an increase in intrarenal Ang II or otherwise interact with Ang II and thereby promote hypertension. In this study, the investigators propose to explore the causality of uric acid in affecting blood pressure and, importantly, to begin to explore the underlying mechanism of such a response using our unique protocol in human subjects. 