Key result
In male rats, 2-methoxyestradiol reduced hypertension, cardiac hypertrophy, proteinuria, and mesangial expansion induced by chronic Angiotensin II infusions.
Why the study?
Estradiol may antagonize the adverse cardiovascular effects of Ang II, but the effects of its nonestrogenic metabolite 2-methoxyestradiol on Ang II-induced cardiovascular and renal injury were unknown.
Does 2-methoxyestradiol reduce hypertension and cardiovascular remodeling in rat models of renin-angiotensin system activation?
Does 2-methoxyestradiol reduce hypertension and cardiovascular remodeling in rat models of renin-angiotensin system activation?
2-methoxyestradiol protects against cardiovascular and renal injury due to chronic activation of the renin-angiotensin system in rat models.
2-ME effects on Ang II injury in rats do not inform practice; leaves open translation to human cardiovascular research.
Estradiol may antagonize the adverse cardiovascular effects of angiotensin II (Ang II). We investigated the effects of 2-methoxyestradiol (2-ME), a nonestrogenic estradiol metabolite, on Ang II-induced cardiovascular and renal injury in male rats. First, we determined the effects of 2-ME on Ang II-induced acute changes in blood pressure, renal hemodynamics, and excretory function. Next, we investigated the effects of 2-ME and 2-hydroxyestardiol (2-HE) on hypertension and cardiovascular and renal injury induced by chronic infusion of Ang II. Furthermore, the effects of 2-ME on blood pressure and cardiovascular remodeling in the constricted aorta (CA) rat model and on isoproterenol-induced (ISO) cardiac hypertrophy and fibrosis were examined. 2-ME had no effects on Ang II-induced acute changes in blood pressure, renal hemodynamics, or glomerular filtration rate. Both 2-ME and 2-HE reduced hypertension, cardiac hypertrophy, proteinuria, and mesangial expansion induced by chronic Ang II infusions. In CA rats, 2-ME attenuated cardiac hypertrophy and fibrosis and reduced elevated blood pressure above the constriction. Notably, 2-ME reduced both pressure-dependent (above constriction) and pressure-independent (below constriction) vascular remodeling. 2-ME had no effects on ISO-induced renin release yet reduced ISO-induced cardiac hypertrophy and fibrosis. This study shows that 2-ME protects against cardiovascular and renal injury due to chronic activation of the renin-angiotensin system. This study reports for the first time that in vivo 2-ME reduces trophic (pressure-independent) effects of Ang II and related cardiac and vascular remodeling.
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Salah et al. (2019) studied Angiotensin II-induced hypertension, cardiovascular remodeling, and renal injury. 2-methoxyestradiol (2-ME) was evaluated on Blood pressure, cardiac hypertrophy, proteinuria, and mesangial expansion. In male rats, 2-methoxyestradiol reduced hypertension, cardiac hypertrophy, proteinuria, and mesangial expansion induced by chronic Angiotensin II infusions.
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