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-estradiol downregulates tissue angiotensin converting enzyme and angiotensin II type-1 receptor in female rats
1 Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
* To whom correspondence should be addressed. E-mail: fleenen{at}ottawaheart.ca.
Estrogens have been implicated in both the worsening of and protection from cardiovascular disease. The effects of 17
-estradiol (E2) on the cardiovascular system may be mediated - at least in part - by its modulation of local tissue renin angiotensin systems (RASs). We assessed two critical components - angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) - in the heart, lung, abdominal aorta, adrenal, kidney and brain in four groups of female Wistar rats (n=5-6/group): 1) Sham-ovariectomized, 2) ovariectomized (OVX) treated with subcutaneous (s.c). vehicle; 3) OVX treated with 25 µg/day ('regular') E2 s.c. and 4) OVX treated with 250 µg/day ('high') s.c. E2 for 2 or 5 weeks. After 2 weeks, plasma ACE activity was not altered by OVX, but it was 34-38% lower in OVX+reg E2 and OVX+high E2 rats compared to Sham-OVX rats and these decreases were no longer present after 5 weeks. After 5 weeks, OVX alone increased ACE activity and binding densities, and AT1R binding densities by 15-100% in RV, LV, kidney, lung, abdominal aorta, adrenal and several cardiovascular regulatory nuclei in the brain. These effects were for the most part prevented by regular E2 replacement and reversed to decreases by high E2 treatment. This regulation of tissue ACE and AT1R is significant as the activity of these tissue RASs contributes to the pathogenesis and/or progression of e.g. hypertension, atherosclerosis and LV remodeling following myocardial infarction.
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