The present study tested the hypothesis that 17-estradiol (E2) inhibits the increases in angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT₁R) in the brain and heart following myocardial infarction (MI) and thereby inhibits the development of left ventricular (LV) dysfunction post-MI. Age-matched female Wistar rats underwent one of three treatments: 1) no surgery (ovary-intact), 2) ovariectomy (OVX) plus subcutaneous vehicle treatment or 3) OVX plus subcutaneous high E2 treatment. Two weeks later, rats were randomly assigned to coronary artery ligation (MI) or sham-operation and followed for 3 weeks. E2 status did not affect LV function in sham rats. At 2-3 weeks post-MI, the impairment of LV function was similar across MI groups, as measured by echocardiography and direct LV catheterization. LV ACE mRNA abundance and activity were increased several fold compared to respective sham groups in all MI groups and to similar levels across MI groups. In most of the brain nuclei studied, ACE and AT₁R densities increased post-MI. Unexpectedly, compared to their respective sham groups the relative increase was the clearest (+20-40%) in the OVX+high E2 MI group, somewhat less (+10-15%) in the ovary-intact MI group, and the least (<10-15%) in the OVX+veh MI group. However, since in the sham rats brain ACE and AT₁R densities increased in the OVX+veh group and decreased in the OVX+high E2 group as compared to the ovary-intact group, actual ACE and AT₁R densities in most brain nuclei were modestly higher (<20%) in OVX+veh MI rats compared to the other two MI groups. Thus, E2 does not inhibit the upregulation of ACE in the LV post-MI, and actually amplifies the percent increases in ACE and AT₁R densities in brain nuclei post-MI despite the down-regulation E2 causes in sham rats. Consistent with these minor variations in the tissue RAS, during the initial post-MI phase E2 appears not to confer any benefit or detriment to the development of LV dysfunction.