Abstract
Gender differences in cardiovascular disease suggest that estrogens provide cardioprotective effects. Recent clinical trials, however, appear to dispute this hypothesis. We have recently reported that angiotensin-(1–7) (Ang-(1–7)), the product of angiotensin converting enzyme 2 (ACE2) cleavage of angiotensin II, can attenuate aspects of cardiac remodeling in the deoxycorticosterone acetate (DOCA)-salt model of mineralocorticoid hypertension, and others have reported that estrogens increase circulating and tissue levels of ACE2 and Ang-(1–7) in rodents. Here we investigated the effects of chronic 17-beta-estradiol (E2, the most prominent endogenous estrogen) treatment on cardiac remodeling during DOCA-salt hypertension. Female SD rats were ovari- and uninephrectomized, and a 40 mg pellet of DOCA was implanted subcutaneously. Half of these animals also received a subcutaneous 0.1 mg pellet of E2 and DOCA groups were maintained on 0.9% NaCL. DOCA treatment, with or without estrogen, significantly increased blood pressure and ventricular mass. Interstitial fibrosis doubled with DOCA treatment, and this effect was normalized by E2 co-treatment. Together with our previous studies, we conclude that E2 modulates DOCA-induced cardiac fibrosis, and hypothesize that these effects may be mediated through modulation of the ACE2 / Ang-(1–7) axis.
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