Submitted on November 11, 2007
Accepted on January 29, 2008
Effect of dietary sodium on estrogen regulation of blood pressure in Dahl salt-sensitive rats
Wei Zheng1, Hong Ji2*, Christine Maric2, Xie Wu2, and Kathryn Sandberg2
1 Center for the Study of Sex Differences in Health, Aging and Disease, Georgetown University, Washington, District of Columbia, United States; Medicine, Georgetown University, Washington, District of Columbia, United States
2 Center for the Study of Sex Differences in Health, Aging and Disease, Georgetown University, Washington, District of Columbia, United States
* To whom correspondence should be addressed. E-mail: jih{at}georgetown.edu.
The effects of high sodium (HS) and normal sodium (NS) diets on ovarian hormone modulation of mean arterial pressure (MAP) were examined in Dahl salt-resistant (DR) and salt-sensitive (DS) rats. Ovariectomy increased MAP (OVX-Sham) to a greater extent in DS maintained for 2 weeks on HS (22 mmHg) compared to NS (6 mmHg). Ovariectomy had no effect on MAP in DR on NS but did increase MAP on HS (10 mmHg). On HS: glomerular filtration rate (GFR) was 36% less in DS-Sham than DR-Sham; ovariectomy increased GFR in both strains by 1.4-1.5-fold; glomerular angiotensin type 1 receptor (AT1R) densities were 1.6-fold higher in DS-Sham than DR-Sham; ovariectomy increased glomerular AT1R densities by 1.3-fold in DR but had no effect in DS; 17
-estradiol (E2) downregulated adrenal AT1R densities in both strains on either diet; ovariectomy reduced estrogen receptor-alpha (ER
) protein expression in the renal cortex by 40-50% though renal ER expression was 34% lower in DS than DR. These observed effects of gonadectomy were prevented by E2-treatment, suggesting E2 deficiency mediates effects of ovariectomy on MAP, GFR, AT1R densities and renal ER protein expression. In conclusion, ovariectomy-induced increases in MAP are augmented by HS diet in both strains and this effect is not mediated by a reduction in GFR. Aberrant renal AT1R regulation and reduced renal ER expression are potential contributors to the hypertensive effects of E2 deficiency in DS. These findings have implications for women with salt-sensitive hypertension and women who are E2 deficient, such as postmenopausal women.
