281
Views
8
CrossRef citations to date
0
Altmetric
Research Article

Effect of estradiol on the expression of renal sodium transporters in rats

, , , , , , , , & show all
Pages 265-273 | Received 14 Nov 2011, Accepted 01 Mar 2012, Published online: 05 Jun 2012
 

ABSTRACT

Background Although estradiol has been thought to perform an important role in blood pressure regulation, the effects of estradiol on the expression of renal sodium transporters are not fully understood.

Methods Female Sprague–Dawley rats were treated with 17β-estradiol or vehicle for 10 days after ovariectomy, and after both ovariectomy and adrenalectomy to eliminate the effect of aldosterone.

Results In the ovariectomized (OVX) rats, estradiol decreased the abundance of the Na-K-2Cl cotransporter (NKCC2) (31.5% of control (OVX), p < 0.01), Na-Cl cotransporter (NCC) proteins (40.5% of control (OVX), p < 0.01) and α- and γ-subunits of the epithelial sodium channel (ENaC) (44.7% and 11.0% of control (OVX), p < 0.01). Estradiol also reduced plasma aldosterone levels (OVX + 17β-estradiol vs. OVX, 116.3 ± 44.4 vs. 184.2 ± 33.4 pmol/l, p < 0.05) and systolic blood pressure (OVX + 17β-estradiol vs. OVX, 115 ± 4 vs. 132 ± 2 mmHg, p < 0.05). In rats having undergone adrenalectomy and ovariectomy, estradiol did not reduce systolic blood pressure, or the expression of sodium transporters.

Conclusion Estradiol decreased systolic blood pressure, plasma aldosterone levels, and the expression of renal sodium transporters. After aldosterone was eliminated, estradiol did not affect blood pressure or the expression of sodium transporters, which indicates that the effect of estradiol on the renal sodium transporters is at least partly influenced by aldosterone.

ACKNOWLEDGEMENTS

Some parts of this study were presented at the 2008 American Society of Nephrology Annual Meeting and the 2008 Federation of American Societies for Experimental Biology Meeting.

Conflict of interest The authors report no conflict of interest. The authors alone are responsible for the content and writing of this paper.

Source of funding This work was supported by Grant No 06-2007-1529 from the SNUH (Seoul National University Hospital) Research Fund.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.