Rapid Relaxant Effects of 17β-estradiol though Endothelium-dependent and-independent Mechanisms in Rat Aorta

[Objective] This research is aimed to investigate the endothelium-dependent and endothelium-independent vasodilative effect of 17β-estradiol (E2) and its mechanism. [Methods] We examined the isometric tension of aortic ring sections isolated from female Sprague-Dawley rats in vitro perfusion using a dual myograph system. [Result]Our research demonstrates that E2 induced concentration-dependent relaxation in precontracted female rat aortic rings. The relaxation induced by E2(10-9～10-6 mol/L) was significantly greater in the rings with endothelium than in the rings without endothelium, While there was no difference of the relaxation in the rings with or without endothelium when the concentration of E2 was increased to 10-5 mol/L. The relaxation was significantly attenuated by preincubation with L-NAME, methylene blue, tamoxifen and methyl-β-cyclodextrin. Incubation with E2(10-5 mol/L) inhibited the concentration-dependent contraction induced by CaCl2 in high K+, Ca2+ free medium in denuded rings. [Conclusion]The rapid aortic arterial relaxation induced by E2 is endothelium-dependent and related to estrogen receptor-mediated release of nitric oxide, and the integrity of caveolae construction is also required. Our research also demonstrates that E2 at the higher concentration induces relaxation mainly by direct calcium antagonistic effect, which is endothelium-independent.