Activation of the GPR30 receptor inhibits aldosterone-induced cardiac hypertrophy

DI MATTÍA RA; AIELLO EA; ORLOWSKI A

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencia; 2017

GPR30 was first described as a membrane orphan G protein-coupled receptor. Later it was demonstrated that estrogen can act as a receptor ligand. It has been reported that the activation of GPR30 is cardioprotective. The administration of its synthetic ligand G1 reduced the infarct size in ischemia-reperfusion, attenuated heart failure and induced a decrease in perivascular fibrosis. The steroid hormone aldosterone (Ald) plays a classic role acting through mineralocorticoid receptor (MR) and its activation on the cardiovascular system generates cardiac hypertrophy, fibrosis and heart failure. It has been recently proposed that certain non-genomic effects of Ald are due to the activation of GPR30. However these results are in contraposition with the beneficial effects of GPR30 activation. The aim of this work was to evaluate the role of GPR30 activation in a model of hypertrophy induced by Ald. We cultured neonatal rat cardiomyocytes (NRCM) from 1-3 days Wistar rats and treated them for 48 hours with Ald (10nM), G1 (1uM) or the combination of both.Hypertrophy caused by Ald was attenuated by the co-treatment with G1 (cellular area % respect to control, Control: 1±0.07, n=9; Ald: 1.33±0.05*, n=8; Ald + G1: 0.93±0.05, n=7; *p