Ethinylestradiol does not enhance the expression of nitric oxide synthase in bovine endothelial cells but increases the release of bioactive nitric oxide by inhibiting superoxide anion production

摘要: Abstract Estradiol is known to exert a protective effect against the development of atherosclerosis, but mechanism by which this protection mediated unclear. Since animal studies strongly suggest that production endothelium-derived relaxing factor enhanced estradiol, we have examined estrogens on nitric oxide (NO) synthase (NOS) activity, protein, and mRNA in cultured bovine aortic endothelial cells. In reporter cells rich guanylate cyclase, it has been observed long-term treatment (> or = 24 hr) with ethinylestradiol (EE2) dose-dependently increased cyclase-activating activity conditioned medium However, conversion L-[14C]arginine L-[14C]citrulline cell homogenate quantification nitrite nitrate released intact did not reveal any change NOS induced EE2 treatment. Similarly, Western Northern blot analyses protein content response EE2. dose- time-dependently decreased superoxide anion an EC50 value (0.1 nM) close (0.5 nM). Both these effects were completely prevented antiestrogens tamoxifen RU54876. Thus, endothelium exposure appears induce receptor-mediated antioxidant enhances biological NO. These could account at least part for vascular properties hormones.