The Role Of Oxidative Stress On Blood Pressure In Dahl Salt-sensitive Postmenopausal Rats

Objective:Postmenopausal women have greater salt sensitivity of blood pressure(BP)than premenopausal women.However,the mechanisms responsible for the postmenopausal salt-sensitive hypertension are not to be fully elucidated The goal of this study was to test the hypothesis that oxidative stress in female Dahl salt-sensitive rats on high salt diet contributes to the development of postmenopausal hypertension.Methods:Intact(INT)or ovariectomized(OVX)female DS rats were treated with antioxidant or oxidant,tempol or molsidomine in drinking water or vehicle for 7 days with low salt diet and 14 days with high salt diet Mean arterial pressure(MAP)was measured by radiotelemetry.Proteinuria,urinary nitric oxide and 8-isoprostaine excretion,superoxide production and the expression of the main antioxidant enzymes,Cu/Zn superoxide dismutase(SOD),catalse and glutathione peroxidase in the kidney were determinedResults:The body weight and basal BP on low salt diet was higher in OVX females,accompanied by the lower NOx excretion.High salt challenge increased BP and proteinuria,and decreased NOx excretion in both INT and OVX females.Tempol or molsidomine failed to reduce or increase BP and proteinuria on high salt diet in either INT or OVX females,but on low salt diet molsidomine decreased BP with increase in NOx excretion in INT females only.F2-isoprostane excretion and renal NADPH oxidase activity were unaffected by tempol and molsidomine on high salt diet in either INT or OVX females.In INT females,renal antioxidant enzymes,Cu/Zn-SOD,catalase,and glutathione peroxidase protein expression were significantly decreased in response to tempol and molsidomine,but only Cu/Zn-SOD and glutathione peroxidase expression were decreased with tempol in OVX females.Conclusion:oxidative stress has a little effect on BP in INT and OVX female DS rats,and the lack of a pressor reslponse to oxidative stress in salt sensit:ive postmenopausal hypertension is independent of the changes in renal antioxidant enzymes.