Selective activation of the G-protein-coupled estrogen receptor (GPER) decreases cardiac contractility through inhibition of the L-type calcium channel (ICa) via Nitric Oxide Synthase.

IBAÑEZ AM; ESPEJO MS; AIELLO EA; DIAZ ZEGARRA LA; DE GIUSTI VC

Rosario

Congreso; Reunión anual de la Sociedad Argentina de Fisiología (SAFIS); 2019

GPER was described as an orphan membrane receptorassociated with protein G. Years later, estradiol wasproposed as a ligand. The activation of GPER by itssynthetic agonist G1 has cardioprotective effects.However, the mechanisms involved in these effects havenot been fully clarified. The objective is to evaluate therole of GPER on baseline cardiac contractility. Rat heartventricular myocytes loaded with the fluorescent calciumindicator FURA-2 were used. Sarcomeric shortening (SS)and transient changes in intracellular calciumconcentration (Ca2+i) were measured by video cameraand epifluorescence, respectively. Calcium influx throughthe L-type channel (ICa) was evaluated with the patchclamptechnique. * indicates p0.05). We conclude thatthe selective activation of cardiac GPER induces adecrease in contractility as a consequence of theinhibition of ICa, through activated NOS, however otherintermediaries are not ruled out.