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Endocrinology Vol. 144, No. 7 3251-3261
Copyright © 2003 by The Endocrine Society

Estrogen Regulates Adrenal Angiotensin AT1 Receptors by Modulating AT1 Receptor Translation

Zheng Wu, Christine Maric, Darren M. Roesch, Wei Zheng, Joseph G. Verbalis and Kathryn Sandberg

Departments of Physiology and Biophysics (Z.W., K.S.) and Medicine (C.M., D.M.R., W.Z., J.G.V., K.S.), Georgetown University, Washington, D.C. 20007

Address all correspondence and requests for reprints to: Kathryn Sandberg, Ph.D., Building D, Room 394, Georgetown University Medical Center, 4000 Reservoir Road, NW, Washington, D.C. 20007. E-mail: sandberg{at}georgetown.edu

Hypertension and associated cardiovascular disease increase after menopause. Angiotensin AT1 receptor (AT1R) antagonists are effective treatments, in part, by inhibiting angiotensin II (Ang II)-induced aldosterone release from the adrenal zona glomerulosa (ZG). Estrogen decreases the number of AT1Rs in the adrenal gland and attenuates acute Ang II-induced aldosterone release. Here, we examined the effects of 17ß-estradiol (E2) on AT1R gene regulation in the rat adrenal cortex (AC). Female rats were ovariectomized and injected with vehicle or E2. Immunohistochemistry revealed the presence of both estrogen receptor (ER){alpha} and ERß in the ZG, and E2 treatment increased the intensity of their nuclear staining. Under conditions in which AT1R maximal binding capacity was decreased by 46%, chronic miniosmotic pump Ang II-induced aldosterone secretion was reduced by 43%. E2 treatment had no effect on AT1aR and AT1bR mRNA levels in the AC, whereas the AT1R mRNA polysome distribution in sucrose gradients was shifted to lighter fractions, indicating that E2 treatment reduces AT1R translation. RNA binding proteins (RBPs) in AC extracts formed complexes with the 5' leader sequence (5'LS), coding region, and the 3'-untranslated region (3'UTR); however, only the activity of 5'LS RBPs was regulated by E2 treatment. These data suggest that E2, acting through its receptors in the ZG, reduces AT1R density and Ang II-induced aldosterone release, primarily by inhibiting AT1R translation, possibly by blocking ribosomal scanning caused by increased steric hindrance from 5'LS RBPs. Dysregulation of this posttranscriptional mechanism may contribute to the increased incidence of cardiovascular disease associated with menopause.




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