Abstract
Although recent studies suggest that estrogen may alter renal expression of certain sodium transporters, conflicting results make its effects on the regulation of renal sodium transporters complicated. To determine the effect of estrogen on the expression of major sodium transporters, we performed semiquantitative immunoblotting analysis of the kidneys from ovariectomized (OVX) Sprague‐Dawley rats treated with (n=6) or without (n=5) high dose of 17β‐estradiol benzoate (E2) (14mcg/100g BW) for 10 days. Physiologic data including body weight (BW), blood pressure (BP), fractional excretion of sodium (FENa) and plasma aldosterone level were also measured.BP showed no difference between two groups. BW was 278 ± 20 g in E2‐replaced rats and 311 ±15 g in OVX rats(p=0.028). FENa of the E2‐replaced rats increased without significant difference (E2 vs. OVX, 0.57 ± 0.22% vs. 0.36 ± 0.19%; mean ± SD, p=0.14). Plasma aldosterone level was 179 ± 125 pg/ml in E2‐replaced rats and 315 ± 218 pg/ml in OVX rats(p=0.20). Administration of E2 led to significant decrease in the protein abundances for Na‐Cl cotransporter, Na‐K‐2Cl cotransporter, the Na‐K‐ATPase, α‐ and γ‐subunits of ENaC in the OVX rats (66%, 32%, 52%, 59% and 49% of control, respectively; p<0.05).E2 replacement to OVX rats resulted in down‐regulation of major renal sodium transporters, which might be associated with reduced plasma aldosterone level.
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