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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 Health Sciences Center, Albuquerque, NM; Pathologisches Institut (K.A.), Universitätsklinikum Erlangen, Germany; Klinik für Herzchirurgie (M.G.), Stadtspital Triemli, Zürich, Switzerland; and Department of Internal Medicine (D.J.C.), Touchstone Diabetes Center, University of Texas, Southwestern Medical Center, Dallas, Tex.
Correspondence to Matthias Barton, Departement für Innere Medizin, Klinik und Poliklinik für Innere Medizin, Universitätsspital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland. E-mail barton{at}usz.ch
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.
Key Words: adipocytes atherosclerosis sex differences vascular disease metabolic syndrome
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