The aim of the studies described in this thesis was to examine the effects of UA on endothelial function and investigate whether UA has the potential to reverse endothelial dysfunction induced by low-density lipoprotein (LDL). Mesenteric arteries were isolated from Wistar-Kyoto rats and the responses to vasoconstrictor (PE, phenylephrine) and endothelium-dependent (ACh, acetylcholine) and – independent (SNP, sodium nitroprusside) vasodilators examined using perfusion myography. Exposure to the vascular lumen to increasing concentrations of UA (200, 400, 600μM) or vehicle solution had no effect upon the responses to PE, ACh or SNP.  This implied that, in this model, acute exposure to elevated UA does not impair endothelial function. In contrast, when the lumen was perfused with increasing concentrations of LDL (250, 500 and 1000μg/ml), maximal vasodilation towards resting diameter in response to ACh was reduced to 42.6, 33.6 and 21.7% respectively. The failure of the NOS inhibitor L-NAME to further impair vasodilation implied that major effect of LDL was to abolish endothelium-dependent NO-mediated vasodilation. Supplementing the perfusing LDL solution with 1mM L-arginine restored endothelium-dependent responses, implying that the LDL-induced endothelial dysfunction was in part explained by a disruption of L-arginine metabolism. Supplementation with the extracellular O₂^- scavenger, superoxide dismutase (SOD) did not prevent the deleterious action of LDL. The experiments then focused on investigating the potential mechanisms by which UA prevented LDL-induced endothelial dysfunction. Isolated rings of thoracic aorta from Wistar-Kyoto rats were mounted in a wire myography and exposed to ACh in the presence of varying concentrations of UA and 250μg/ml LDL.  The superfusate was then transferred to endothelium-denuded rings and caused significant vasodilation in previously unresponsive ring segments. The extent of the vasodilation in response to the transferred solution was dependent on the concentration of UA and ox-Hb sensitive.  The decay in vasodilator response if the exposure of the denuded ring was delayed had a half-life of 29 minutes. These results implied that the stimulation of an endothelium-intact vessel by ACh in the presence of both UA and LDL results in the formation of an endothelium-independent vasodilator that releases NO and may be a derivative of UA.