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Estrogen Regulates Adrenal Angiotensin Type 1 Receptors by Modulating Adrenal Angiotensin Levels

Departments of Physiology and Biophysics (Z.W., K.S.) and Medicine (W.Z., K.S.), Georgetown University, Washington, DC 20057

Address all correspondence and requests for reprints to: Kathryn Sandberg, Ph.D., Building D, Room 394, Georgetown University Medical Center, 4000 Reservoir Road Northwest, Washington, DC 20057. E-mail: sandberg{at}georgetown.edu.

Estrogen inhibits adrenal angiotensin type 1 receptor (AT₁R) binding sites and attenuates the adrenal responsivity to angiotensin II (Ang II). Ang II modulates AT₁R expression. Here, we determined if estrogen-induced down-regulation of adrenal AT₁Rs involves modulation of adrenal Ang II. Female rats were ovariectomized (OVX) and injected with 17ß-estradiol benzoate (E₂; 40 µg/kg) or vehicle for 7 d. Adrenal Ang II was separated from other angiotensin peptides by HPLC and measured by RIA. Scatchard analysis of radioligand binding curves showed that E₂ or captopril (Cap; 0.5 g/liter water) significantly reduced adrenal AT₁R binding (maximum binding capacity) by 22% and 19%, respectively, compared with OVX (276 ± 2.09 fmol/mg protein). E₂ and Cap lowered adrenal Ang II levels by 39% and 21%, respectively, compared with OVX (4.10 ± 0.44 pmol/g). E₂ caused no further reductions in adrenal AT₁R binding or in Ang II levels in Cap-treated OVX rats. High-dose Ang II infusion (1000 ng/kg·min) increased adrenal Ang II levels by 71% and lowered AT₁R binding by 18%. Under these infusion conditions, E₂ did not reduce adrenal Ang II or AT₁R binding. No differences in AT₁R affinity (dissociation constant) were observed among groups. These data suggest that E₂ regulates the number of adrenal AT₁R binding sites indirectly by modulating adrenal Ang II.

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