| Abstrakt: |
Objective:Because we showed recently that estrogen replacement prevents prostaglandin H synthase (PGHS)—dependent vasoconstriction in rats, the aim of this study was to determine how estradiol affects production of PGHS-dependent eicosanoids.Methods:Cultured bovine coronary microvascular endothelial cells were exposed to physiologic levels of 17β-estradiol (0.01nM [about 2.7 pg/mL], 0.1 nM [about 27 pg/mL], or 1.0 nM [about 270 pg/mL]) for 4, 8, or 24 hours. Thromboxane (TXA2), prostacyclin (PGI2), and nitric oxide (NO) were measured as their stable metabolites, thromboxane B2 (TXB2), 6-keto prostaglandin F1α (6-keto PGF1α), and nitrite (NO2), respectively.Results:Estradiol had no effect on nitrite production. However, exposure to 0.1 nM and 1.0 nM estradiol for 24 hours reduced TXB2 production to 67 ± 16% and 69 ± 12% of control, respectively. Furthermore, 0.1 nM and 1.0 nM estradiol also reduced production of 6-keto PGF1α to 35 ± 19% and 17 ± 11% of control, respectively. Prostaglandin H synthase expression was not altered by estradiol. However, the estrogen receptor inhibitor, tamoxifen, reversed the inhibitory effect of estradiol.Conclusion:Estradiol acts through a receptor-dependent process to decrease PGHS-dependent products, thus further elucidating this novel effect of estradiol on the vascular system. [ABSTRACT FROM PUBLISHER] |
Full text from SpringerLink