Regulatory Role of G Protein–Coupled Estrogen Receptor for Vascular Function and Obesity

Author:

Haas Elvira1,Bhattacharya Indranil1,Brailoiu Eugen1,Damjanović Marlen1,Brailoiu G. Cristina1,Gao Xin1,Mueller-Guerre Laurence1,Marjon Nicole A.1,Gut André1,Minotti Roberta1,Meyer Matthias R.1,Amann Kerstin1,Ammann Emerita1,Perez-Dominguez Ana1,Genoni Michele1,Clegg Deborah J.1,Dun Nae J.1,Resta Thomas C.1,Prossnitz Eric R.1,Barton Matthias1

Affiliation:

1. From the Departement für Innere Medizin (E.H., I.B., M.D., L.M.-G., A.G., R.M., M.R.M., E.A., A.P.-D., M.B.), Klinik und Poliklinik für Innere Medizin; and Klinik für Herz- und Gefässchirurgie (M.G.), Universitätsspital Zürich, Switzerland; Department of Pharmacology (E.B., G.C.B., X.G., N.J.D.), Temple University School of Medicine, Philadelphia, Pa; Department of Cell Biology and Physiology (N.A.M., T.C.R., E.R.P.) and University of New Mexico Cancer Center (E.R.P.), University of New Mexico...

Abstract

We found that the selective stimulation of the intracellular, transmembrane G protein–coupled estrogen receptor (GPER), also known as GPR30, acutely lowers blood pressure after infusion in normotensive rats and dilates both rodent and human arterial blood vessels. Stimulation of GPER blocks vasoconstrictor-induced changes in intracellular calcium concentrations and vascular tone, as well as serum-stimulated cell proliferation of human vascular smooth muscle cells. Deletion of the GPER gene in mice abrogates vascular effects of GPER activation and is associated with visceral obesity. These findings suggest novel roles for GPER in protecting from cardiovascular disease and obesity.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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