Cardiovascular Research Institute, Kyungpook National University School of Medicine, Daegu, 700-422, Republic of Korea.
Naunyn Schmiedebergs Arch Pharmacol. 2012 Sep;385(9):945-8. doi: 10.1007/s00210-012-0770-y. Epub 2012 Jun 12.
17β-Estradiol (E2) exerts rapid non-genomic vascular effects through activation of its plasma membrane receptors. We tested the hypothesis that E2 induces vasorelaxation through activation of the G-protein-coupled receptor 30 (GPR30) in rat aorta. Rat aortic rings were mounted in organ baths and subjected to contraction followed by relaxation. Whether endothelium was intact or denuded, both E2 and G1, a GPR30 agonist, induced vasorelaxation in concentration-dependent manners. Although G15, a specific GPR30 antagonist, blocked G1-induced vasorelaxation, it did not block E2-induced vasorelaxation. In conclusion, 17β-estradiol induces vasorelaxation in a GPR30-independent manner in rat aorta.
17β-雌二醇（E2）通过其质膜受体的激活发挥快速非基因组血管作用。我们检验了以下假说，即 E2 通过激活大鼠主动脉中的 G 蛋白偶联受体 30（GPR30）诱导血管舒张。大鼠主动脉环被安装在器官浴中，并进行收缩，然后进行松弛。无论内皮是否完整或去除，E2 和 G1（GPR30 激动剂）均以浓度依赖性方式诱导血管舒张。尽管 G15（一种特异性 GPR30 拮抗剂）阻断了 G1 诱导的血管舒张，但它并未阻断 E2 诱导的血管舒张。总之，17β-雌二醇以 GPR30 不依赖的方式诱导大鼠主动脉血管舒张。
