17β-Estradiol induces vasorelaxation in a G-protein-coupled receptor 30-independent manner
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 sub...
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Veröffentlicht in: | Naunyn-Schmiedeberg's archives of pharmacology 2012-09, Vol.385 (9), p.945-948 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | 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. |
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ISSN: | 0028-1298 1432-1912 |
DOI: | 10.1007/s00210-012-0770-y |