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Am J Physiol Regul Integr Comp Physiol (April 4, 2002). doi:10.1152/ajpregu.00573.2001
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Articles in PresS, published online ahead of print April 4, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00573.2001
Submitted on September 19, 2001
Accepted on March 28, 2002

17-ß Estradiol Decreases Hypoxic Induction of Erythropoietin Gene Expression

Harshini Mukundan1*, Thomas C Resta1, and Nancy L Kanagy1

1 Department of Cell Biology and Physiology, University of New Mexico, Albuquerque, New Mexico, USA

* To whom correspondence should be addressed. E-mail: hmukundan{at}salud.unm.edu.

Exposure to chronic hypoxia induces erythropoietin (EPO) production to facilitate oxygen delivery to hypoxic tissues. Previous studies from our laboratory found that ovariectomy (OVX) exacerbates the polycythemic response to hypoxia and treatment with 17-ß estradiol (E2-ß) inhibits this effect. We hypothesized that E2-ß decreases EPO gene expression during hypoxia. Since E2-ß can induce nitric oxide (NO) production and NO can attenuate EPO synthesis, we further hypothesized E2-ß inhibition of EPO gene expression is mediated by NO. These hypotheses were tested in OVX catheterized rats treated with E2-ß (20 µg/day) or vehicle for 14 days and exposed to 8 or 12 hours of hypoxia (12% O2) or normoxia. We found that E2-ß treatment significantly decreased EPO synthesis and gene expression during hypoxia. E2-ß-treatment did not induce endothelial nitric oxide synthase (eNOS) expression in the kidney but potentiated hypoxia-induced increases in plasma nitrates. We conclude that E2-ß decreases hypoxic induction of EPO. However, this effect does not appear to be related to changes in renal eNOS expression.




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