Activation of the GPR30 receptor inhibits aldosterone-induced cardiac hypertrophy

ORLOWSKI A; DI MATTÍA RA; AIELLO EA

Chicago

Congreso; Experimental Biology Congress; 2017

The hormone aldosterone (Ald) plays classic role acting through mineralocorticoids receptors (MR) located in the cytosol, which act as ligand-induced transcription factors. Many cardiac deleterious effects of Ald are mediated by the activation of the MR. However, activated MR can also elicit additional non-genomic effects. In addition, it has been recently proposed that certain non-genomic effects of Ald were due to the activation of the G protein-coupled receptor 30 (GPR30). It has been reported that the activation of GPR30 is cardioprotective. The administration of the GPR30 synthetic agonist G1 reduced the infarct size, diminished left ventricular wall thickness, attenuated heart failure and induced a decrease in perivascular fibrosis. The aim of this study was to investigate the potential cardioprotective effects of GPR30 on Ald-induced hypertrophy in neonatal cardiac myocytes. Consistent with previous reports, dose-dependent response to 24 hs Ald treatment increased cell size (A.U., control: 186±11, n=20; Ald (0.1nM): 185±12, n=22; Ald (1 nM): 202±12, n=17; Ald (10 nM): 260±21*, n=23; Ald (100 nM): 268±17*, n=29; Ald (1000 nM): 275±15*, n=14; * indicates p