[Effects of 17 beta-estradiol on the release of nitric oxide from HUVEC]

The protective mechanism of 17 beta-estradiol on blood vessels was investigated to provide evidences for clinical use of hormone replacement therapy in postmenopausal women.

To observe the effects of 17 beta-estradiol (17 beta-E2), testosterone (T), homocysteine (Hcy), 17 beta-E2 combined with T and 17 beta-E2 combined with Hcy on the production of nitric oxide (NO) released from cultured human umbilical endothelial cells (HUVEC) in vitro.

Preincubation with 10(-9) mol/L 17 beta-E2 8-48 hours significantly enhanced the release of nitric oxide from HUVEC versus the control, but 10(-9) mol/L T had no effects within 48 hours. Pretreatment with 10(-9)-10(-7) mol/L testosterone for 24 hours had no effects on the release of NO from HUVEC versus the control, but 10(-6), 10(-5) mol/L T significantly reduced the release of NO from HUVEC. HUVEC were treated by 10(-9)-10(-5) mol/L 17 beta-E2 and 10(-9)-10(-5) mol/L T respectively for 24 hours. 10(-9), 10(-8) mol/L T had no effects on the beneficial effect of 17 beta-E2 with regard to the production of NO from HUVEC, while 10(-5) mol/L T greatly attenuated the beneficial effect of 17 beta-E2 with regard to the production of NO from HUVEC. Pretreatment with 10(-4)-10(-3) mol/L Hcy for 24 hours greatly inhibited the release of NO from HUVEC. If treated HUVEC with various concentrations of 17 beta-E2 (10(-9), 10(-7), 10(-5) mol/L) and Hcy for 24 hours simultaneously, 10(-9)-10(-7) mol/L 17 beta-E2 can partly eliminate the effects of Hcy on the released of NO from HUVEC.

T can not enhance the release of NO from HUVECs. The effect of 17 beta-E2 combined with T on the release of NO depends on the concentration of both 17 beta-E2 and T. When 17 beta-E2 and T are in low dose, HUVEC can release more NO. Hcy can inhibit the release of NO from HUVEC, concomitant treatment with a low dose of 17 beta-E2 may eliminate the effects of Hcy on HUVEC.