Treatment of cultured human aortic endothelial cells with 17 beta-estradiol enhanced calcium-dependent NO production and increased NO synthase protein levels, whereas testosterone had no effect.
Does 17 beta-estradiol increase NO production and NO synthase protein levels in cultured human aortic endothelial cells?
17 beta-estradiol up-regulates endothelial nitric oxide synthase and enhances NO production in human aortic endothelial cells, providing a potential mechanism for estrogen's cardiovascular effects.
We have examined the effects of sex hormones on calcium-dependent NO production and protein levels of NO synthase in cultured human aortic endothelial cells, which were treated with various doses of 17 beta-estradiol and testosterone for 8-48 h. Treatment with 17 beta-estradiol enhanced calcium-dependent NO production, but testosterone had exerted no effect. Western blot using monoclonal anti-human endothelial NO synthase antibody clarified that increased NO production by 17 beta-estradiol treatment was accompanied by increased NO synthase protein. Our results provide evidence that human endothelial NO synthase can be regulated by estrogens.
Hishikawa et al. (1995) studied Cultured human aortic endothelial cells. 17 beta-estradiol vs. testosterone was evaluated on calcium-dependent NO production and protein levels of NO synthase. Treatment of cultured human aortic endothelial cells with 17 beta-estradiol enhanced calcium-dependent NO production and increased NO synthase protein levels, whereas testosterone had no effect.