Objective　　　 To determine the effects of uncoupling protein 3 (UCP3) knock-out in the vascular endothelium dysfunction in mice induced by high salt intake.　　　 Methods　　　 Male UCP3 knock-out (UCP3 KO

C57BL/6J background) and the matched wild type (WT) mice were divided into 2 groups

the normal salt intake (NS) group and high salt intake (HS) group

10 mice in each group. The former group was given normal diet containing 0.5% salt

while the other group was fed with the diet containing 8% salt

both for 24 weeks. Mesenteric arteries were obtained and stained with dihydroethidium (DHE)

and the level of superoxide anion was observed under fluorescence microscope. Vascular function

including the endothelium-dependent relaxation and endothelium-independent relaxation was measured by wire myography. Blood pressure and tail blood pressure (both systolic and diastolic blood pressures) was detected. The expression of UCP3

and phosphorylated eNOS (p-eNOS) in mice aorta were detected by Western blotting.　　　 Results　　　 Superoxide anion was much higher in mesenteric arteries from WT and UCP3 KO mice from the high salt diet group than from the normal salt diet group (P0.01). While

high salt-fed UCP3 KO mice had markedly higher content of superoxide anion than their corresponding WT littermates (P0.05). Endothelium-dependent relaxation was obviously impaired in mesenteric arteries from both WT and UCP3 KO mice after high salt diet feeding compared with mice having normal diet ( P0.01). Moreover

the impairment was more severe in high salt-fed UCP3 KO mice than their corresponding WT littermates (P0.05). High salt diet feeding resulted in significantly enhanced expression of UCP3 and obviously decreased expression of p-eNOS in the WT mice aorta.　　　 Conclusion　　　 UCP3 ablation shows impaired anti-oxidative stress activity in mice

and high salt diet then further exacerbates the impairment of vascular endothelium function and leads to higher blood pressure.