A high sodium diet in Dahl salt-sensitive rats resulted in significantly greater urinary protein excretion (273 vs 35 mg/d, P<0.05) and lower renal superoxide dismutase than in salt-resistant rats.
Does high sodium intake induce greater oxidative stress and renal damage in Dahl salt-sensitive rats compared to salt-resistant rats?
Salt-sensitive hypertension in Dahl rats is associated with decreased renal SOD and increased oxidative stress and renal damage, highlighting a potential mechanistic role for oxidative stress in salt-sensitive hypertension.
Absolute Event Rate: 273% vs 35%
p-value: p=< 0.05
The roles of oxidative stress and renal superoxide dismutase (SOD) levels and their association with renal damage were studied in Dahl salt-sensitive (S) and salt-resistant (R)/Rapp strain rats during changes in Na intake. After 3 wk of a high (8%)-Na diet in S rats, renal medullary Cu/Zn SOD was 56% lower and Mn SOD was 81% lower than in R high Na-fed rats. After 1, 2, and 3 wk of high Na, urinary excretion of F(2)-isoprostanes, an index of oxidative stress, was significantly greater in S rats compared with R rats. Plasma F(2)-isoprostane concentration increased in the 2-wk S high Na-fed group. After 3 wk, renal cortical and medullary superoxide production was significantly increased in Dahl S rats on high Na intake, and urinary protein excretion, an index of renal damage, was 273 +/- 32 mg/d in S high Na-fed rats and 35 +/- 4 mg/d in R high Na-fed rats (P < 0.05). In conclusion, salt-sensitive hypertension in the S rat is accompanied by marked decreases in renal medullary SOD and greater renal oxidative stress and renal damage than in R rats.
Meng et al. (2002) studied salt-sensitive hypertension. High sodium diet vs. Salt-resistant (R) rats on high sodium diet was evaluated on urinary protein excretion (mg/d) (p=< 0.05). A high sodium diet in Dahl salt-sensitive rats resulted in significantly greater urinary protein excretion (273 vs 35 mg/d, P<0.05) and lower renal superoxide dismutase than in salt-resistant rats.