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1 Hypertension and Vascular Diseae Center, Wake Forest School of Medicine, Winsotn-Salem, North Carolina, United States
* To whom correspondence should be addressed. E-mail: mchappel{at}wfubmc.edu.
This current study determined whether early loss of estrogen influences salt-sensitive changes in blood pressure, renal injury and cardiac hypertrophy, as well as the effects on the circulating renin-angiotensin-aldosterone system (RAAS) in the hypertensive female mRen(2).Lewis strain. Ovariectomy (OVX) of heterozygous mRen(2).Lewis rats on normal salt [NS, 0.5% sodium] increased systolic blood pressure from 137 ± 3 to 177 ± 5 mm Hg (p<0.01) by 15 weeks, but did not change the cardiac to body weight index (CI), proteinuria or creatinine clearance. Maintenance on a high sodium diet (HS, 4%) increased blood pressure [203 ± 4 mm Hg; p<0.01] and proteinuria [3.5 ± 0.3 vs. 6.4 ± 0.7 mg/day; p<0.05], increased CI [4.0 ± 0.1 vs. 5.2 ±0.1 mg/kg; p<0.01] but decreased creatinine clearance [0.89 ± 0.15 vs. 0.54 ± 0.06 ml/min; p<0.05]. OVX exacerbated the effects of salt on the degree of hypertension [230 ± 5 mm Hg], CI [5.6 ± 0.2 mg/kg] and proteinuria [13 ± 3.0 mg/day]. OVX increased urinary excretion of aldosterone approximately two fold in the NS [3.8 ± 0.5 vs. 6.6 ± 0.5 ng/mg creatinine/day; p<0.05] and HS [1.4 ± 0.2 vs. 4.5± 1.0 ng/mg creatinine/day; p<0.05]. Circulating renin, ACE, and Ang II were also significantly increased in the OVX-HS group. These results reveal that the protective effects of estrogen apart from blood pressure were only manifest in the setting of a chronic high salt diet suggesting that the underlying sodium status may have an important influence on the overall effect of reduced estrogen.
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