Maturitas
Volume 25, Issue 2 , Pages 141-147, October 1996

Effect of physiological concentrations of estradiol on PGI2 and NO in endothelial cells

  • Tomi Mikkola

      Affiliations

    • Corresponding Author InformationCorresponding author. Dept. of Obstetrics and Gynecology, Helsinki University Central Hospital, Haartmaninkatu 2. 00290 Helsinki, Finland. Tel: + 358 0 4711; fax: + 358 0 2412192.
    • Department of Obstetrics and Gynecology, University of Helsinki, FIN-00290 Helsinki, Finland
    • ,
  • Varpu Ranta

      Affiliations

    • Department of Obstetrics and Gynecology, University of Helsinki, FIN-00290 Helsinki, Finland
    • ,
  • Arto Orpana

      Affiliations

    • Department of Obstetrics and Gynecology, University of Helsinki, FIN-00290 Helsinki, Finland
    • ,
  • Olavi Ylikorkala

      Affiliations

    • Department of Obstetrics and Gynecology, University of Helsinki, FIN-00290 Helsinki, Finland
    • ,
  • Lasse Viinikka

      Affiliations

    • Department of Clinical Chemistry, University of Helsinki, FIN-00290 Helsinki, Finland

Received 20 March 1996; received in revised form 10 June 1996; accepted 27 June 1996.

Abstract 

Objectives: To elucidate the mechanisms by which estrogens protect against occlusive vascular disorders, we studied the effect of 17β-estradiol on the production of prostacyclin (PGI2) and nitric oxide (NO) in primary cultures of human umbilical vein endothelial cells (HUVECs). Methods: To study the effect of 17β-estradiol on PGI2 production, HUVECs were incubated in the absence and presence of 17β-estradiol (0.01–10 nmol/l) encapsulated within β-cyclodextrin for 12 h in serum-free medium. To study the effect of 17β-estradiol (100 nmol/l) on maximal calcium-dependent NO production, we used different approaches. First, HUVECs were incubated with 2 μmol/l calcium ionophore A23187 with or without 17β-estradiol (100 nmol/l) for 24 h in serum-free medium. Second, HUVECs were preincubated with or without 17β-estradiol (100 nmol/l) for 12 h in medium supplemented with 2% fetal calf serum, and thereafter incubated in serum-free medium with 2 μmol/l of A23187 and with 100 nmol/l of 17β-estradiol (cells which contained 17β-estradiol during the preincubation period as well as cells which did not) or without it (only cells which did not contain 17β-estradiol during the preincubation period) for 6 h or 24 h. Results: 17β-Estradiol (0.1 nmol/l) increased the concentration of 6-keto-prostaglandin F1α, a stable metabolite of PGI2 in the incubation medium, by 16%, and no further increase occurred with higher 17β-estradiol concentrations. The stimulation was prevented by tamoxifen. 17β-Estradiol did not affect NO production in any of our experiments measured as accumulation of nitrate and nitrite in the experimental medium. Conclusions: The stimulatory effect on PGI2 production of physiological concentrations of 17β-estradiol, shown now for the first time, may provide one explanation for the ability of 17β-estradiol to protect against occlusive vascular disorders.

Keywords:  17β-Estradiol, Occlusive vascular disorders, Prostacyclin, Human umbilical vein endothelial cells

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PII: 0378-5122(96)01057-2

Maturitas
Volume 25, Issue 2 , Pages 141-147, October 1996

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