1. Regulatory role of G protein-coupled estrogen receptor for vascular function and obesity
- Author
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Ana Perez-Dominguez, Deborah J. Clegg, Andre Gut, Indranil Bhattacharya, Roberta Minotti, Xin Gao, Emerita Ammann, Eric R. Prossnitz, Laurence Mueller-Guerre, Kerstin Amann, Matthias R. Meyer, Nicole A. Marjon, Matthias Barton, Nae J. Dun, Michele Genoni, Eugen Brailoiu, Elvira Haas, Thomas C. Resta, G. Cristina Brailoiu, and Marlen Damjanović
- Subjects
Male ,medicine.medical_specialty ,Vascular smooth muscle ,Physiology ,medicine.drug_class ,Estrogen receptor ,Vasodilation ,Blood Pressure ,Biology ,Calcium in biology ,Article ,Receptors, G-Protein-Coupled ,Rats, Sprague-Dawley ,Mice ,Internal medicine ,medicine ,Animals ,Humans ,Obesity ,Mammary Arteries ,Receptor ,Estradiol ,Atherosclerosis ,Mice, Mutant Strains ,Rats ,Endocrinology ,Receptors, Estrogen ,Estrogen ,G-Protein Coupled Estrogen Receptor 1 ,Female ,Cardiology and Cardiovascular Medicine ,GPER - 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.
- Published
- 2009