Hormone replacement with estrogen and progestins differentially restored ovariectomy-induced vascular dysfunction linked to renin-angiotensin system regulation in female rats.
Does hormone replacement with estrogen and progestins improve vascular reactivity and modulate the renin-angiotensin system in ovariectomized rats?
Hormone replacement with estrogen and progestins differentially restores vascular dysfunction and modulates the renin-angiotensin system in ovariectomized rats.
The renin–angiotensin system (RAS) is the main endocrine and tissular component responsible for controlling cardiovascular homeostasis, which can be modulated by estrogen levels. This study investigated the effects of hormone treatments with estrogen and progestins on angiotensin-(1-7)-mediated Ang-(1-7) vasodilation in ovariectomized rats and the possible mechanisms involving the RAS. Female Wistar rats were divided into the following groups: sham (SHAM), ovariectomized (OVX), OVX and treated with 17β-estradiol (E2) (OE2), OVX and treated with E2 and drospirenone (OE2 + DRSP), and OVX and treated with medroxyprogesterone (MPA). Hormonal treatment was delivered via gavage for 28 days. Vascular responses to Ang-(1-7) were assessed in isolated aortic rings, and a Western blot of the thoracic aorta was used to determine the protein levels of angiotensin II (Ang II) type-1 receptor (AT1R), Ang II type-2 receptor (AT2R), Ang-(1-7) receptor (Mas), angiotensin-converting enzyme 2 (ACE2), and endothelial nitric oxide synthase (eNOS). The results showed impaired vascular reactivity caused by ovariectomy. Ang-(1-7) induced vasodilation in the OE2, OE2 + DRSP, and MPA-treated groups, while the administration of the AT2R antagonist (PD123319) or the selective Mas antagonist (A779) increased the extent of vasorelaxation induced by Ang-(1-7) in the OVX + MPA group. There were no differences in the aortic levels of AT1R or ACE2 between the groups, but the MPA group showed significantly increased levels of AT2R and eNOS. We concluded that ovariectomy induced vascular dysfunction linked to RAS regulation, and both estrogen (E2) and progestins differentially restored these parameters.
Menezes et al. (2025) studied Ovariectomy-induced vascular dysfunction. Hormone replacement treatment (17β-estradiol, drospirenone, medroxyprogesterone) vs. Sham and untreated ovariectomized rats was evaluated on Vascular responses to Ang-(1-7) and protein levels of RAS components. Hormone replacement with estrogen and progestins differentially restored ovariectomy-induced vascular dysfunction linked to renin-angiotensin system regulation in female rats.