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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Regulation of components of the brain and cardiac renin-angiotensin systems by 17-estradiol after myocardial infarction in female rats

Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

Submitted 8 July 2005 ; accepted in final form 30 January 2006

The present study tested the hypothesis that 17-estradiol (E₂) inhibits increases in angiotensin-converting enzyme (ACE) and ANG II type 1 receptor (AT₁R) in the brain and heart after myocardial infarction (MI) and, thereby, inhibits development of left ventricular (LV) dysfunction after MI. Age-matched female Wistar rats were treated as follows: 1) no surgery (ovary intact), 2) ovariectomy + subcutaneous vehicle treatment (OVX + Veh), or 3) OVX + subcutaneous administration of a high dose of E₂ (OVX + high-E₂). After 2 wk, rats were randomly assigned to coronary artery ligation (MI) and sham operation groups and studied after 3 wk. E₂ status did not affect LV function in sham rats. At 2–3 wk after MI, 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 severalfold in all MI groups compared with respective sham animals and to similar levels across MI groups. In most brain nuclei, ACE and AT₁R densities increased after MI. Unexpectedly, compared with the respective sham groups the relative increase was clearest (20–40%) in OVX + high-E₂ MI rats, somewhat less (10–15%) in ovary-intact MI rats, and least (<10–15%) in OVX + Veh MI rats. However, because in the sham group brain ACE and AT₁R densities increased in the OVX + Veh rats and decreased in the OVX + high-E₂ rats compared with the ovary-intact rats, actual ACE and AT₁R densities in most brain nuclei were modestly higher (<20%) in OVX + Veh MI rats than in the other two MI groups. Thus E₂ does not inhibit upregulation of ACE in the LV after MI and amplifies the percent increases in ACE and AT₁R densities in brain nuclei after MI, despite E₂-induced downregulation in sham rats. Consistent with these minor variations in the tissue renin-angiotensin system, during the initial post-MI phase, E₂ appears not to enhance or hinder the development of LV dysfunction.

ovariectomy; heart failure; estrogens

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