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      Estrogen Does Not Induce the Calcium-Dependent Nitric Oxide Synthase in Cultured Human Uterine Endothelial and Myometrial Smooth Muscle Cells

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          In many tissues, estrogen-induced vasodilatation is mediated, at least in part, by the release of nitric oxide (NO). We determined whether human myometrial endothelial and smooth muscle cells express estrogen receptors (ERs) and whether endothelial NO synthase (eNOS) expression in these cells was affected by 17β-estradiol (10<sup>–13</sup>–10<sup>–6</sup>M). ER was strongly expressed in myometrial smooth muscle cells but was absent from endothelial cells. Expression of eNOS mRNA was strong in endothelial cells, but weak in muscle cells. 17β-estradiol administration for 24 or 72 h failed to increase eNOS in both cell types. Thus, an increase of human uterine blood flow by estrogens appears not to be mediated by stimulation of myometrial eNOS expression.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          24 September 2008
          : 34
          : 4
          : 281-288
          Departments of aObstetrics and Gynecology, bVascular Biology and Thrombosis Research and cPathology, University of Vienna School of Medicine, Vienna, Austria
          159235 J Vasc Res 1997;34:281–288
          © 1997 S. Karger AG, Basel

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          Pages: 8
          Research Paper


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