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.

中文翻译：

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G 蛋白偶联雌激素受体对血管功能和肥胖的调节作用。

我们发现选择性刺激细胞内跨膜 G 蛋白偶联雌激素受体 (GPER)，也称为 GPR30，可在血压正常的大鼠输注后急剧降低血压，并扩张啮齿动物和人类动脉血管。GPER 的刺激阻止血管收缩剂诱导的细胞内钙浓度和血管张力的变化，以及血清刺激的人血管平滑肌细胞的细胞增殖。小鼠中 GPER 基因的缺失消除了 GPER 激活的血管效应，并与内脏肥胖有关。这些发现表明 GPER 在预防心血管疾病和肥胖方面的新作用。