The chronic activation of the G-coupled-estrogen receptor (GPER) prevents ischemia-reperfusion injury in the hearts of ovariectomized rats

SUSANA MOSCA; ALEJANDRO MARTÍN IBAÑEZ; ERNESTO ALEJANDRO AIELLO; LUISA GONZÁLEZ ARBELÁEZ; VERÓNICA DE GIUSTI

Mar del Plata

Congreso; Reunión Anual de la Sociedad Argentina de Fisiología (SAFIS),; 2018

Sociedad Argentina de Fisiología

During menopause women are exposed to an increase in cardiovascular risk, typically associated with lack of estrogens. However classic hormone replacement therapy (HRT) has not been as successful as expected in preventing such pathologies. It has been proved that many of the beneficial effects that estradiol exert on the cardiovascular system are mediated by GPER (G-coupled-estrogen receptor). Recently our group has described a greater damage in ovariectomized rat?s hearts after an ischemia-reperfusion (IR) protocol compared to the control group. The hypothesis of the present work is that specific activation of GPER signaling would be beneficial for cardiovascular health, representing an alternative to HRT. Bilateral ovariectomy was performed in 3-month-old female Wistar rats, which were randomly assigned to undergo a treatment during one month with either G1 (specific agonist of the GPER) (OVXG1) or vehicle (OVXVH). After the treatment, animals were sacrificed and their hearts used for IR protocols. Weight gain (40.73± 5.88 g, n=6 vs 55.27±6.66 g; n=9) and the increase in left ventricle mass (55.94±19.08 mg, n=8 vs 124.93±33.33 mg; n=7) were milder in OVXG1. No differences were detected in systolic blood pressure. Chronic G1 administration prevented mechanic damage after the IR protocol in OVXG1 hearts (Left ventricle developed pressure: 57.98±12.75 % vs 10.28±2.65 %; Left ventricle diastolic end pressure: 55.75±3.99 mmHg vs 12.23±1.28 mmHg, n=5, p