I addition to androgens, estrogens act on the prostate, affecting its development and growth. When applied in some developmental windows, estrogens may lead to prostatites and displastic growth. Tests in vivo executed on rodent prostates showed that the treatment with high doses of exogenous estrogen causes the reduction of the prostate size in addition to alterations on the expression of androgen receptors (AR) and estrogen receptors (ER), while the treatment with low doses results in larger organ. Smooth muscle cells (SMC) are the predominant cell type in the prostatic stroma and influence the epithelium through paracrine mechanisms. They also play roles in extracellular matrix remodeling during growth, regression and tumor invasion. It is known that SMC express the androgen receptor (AR), and that thus respond to the androgens. Androgen deprivation seems to induce them to modify their behavior from contractile to secretory. Our goal was to test the effects of estradiol (E2) on the levels of the AR expression and cellular distribution.  SMC in culture have been treated with different E2 concentrations (1nM, 10nM, 1µM) in the presence and in the absence of testosterone. The interference on the AR expression and the AR localization was studied by Western blotting and immunocytochemistry, respectively. Treatment with estrogen caused a non normotonic effect on the levels of AR protein, with intermediate concentration causing increases in AR amount. The treatment with E2 in the presence of testosterone leads to a decreasing of the protein expression for all concentrations tested. These results have been confirmed by immunocytochemistry, which also showed the same variation for the protein concentration. In addition, it showed a predominant nuclear location, irrespective of the dose. The results of this work indicate that E2 interferes with the expression levels of the AR. Supported by FAPESP.