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本文研究ＥＤＲＦ（ｅｎｄｏｔｈｅｌｉｕｍ－ｄｅｒｉｖｅｄｒｅｌａｘｉｎｇｆａｃｔｏｒ，ＥＤＲＦ）对ＰＥ（ｐｈｅｎｙｌｅｐｈｒｉｎｅ）引起的大鼠主动脉收缩反应的影响。内皮完整和去内皮的大鼠主动脉环悬挂于器官浴槽中，测定血管的张力和收缩速度的变化。所有的实验在消炎痛（ｉｎｄｏｍｅｔｈａｃｉｎ，１０μｍｏｌ／Ｌ）存在下进行。用美兰（ｍｅｔｈｙｌｅｎｅｂｌｕｅ，ＭＢ，１０μｍｏｌ／Ｌ）或左旋硝基精氨酸（ＮＧ－ｎｉｔｒｏ－Ｌ－ａｒｇｉｎｉｎｅ，Ｌ－ＮＮＡ，３０μｍｏｌ／Ｌ）处理内皮完整的大鼠主动脉环，ＰＥ的剂量－收缩张力曲线明显左移，ＥＣ３０值均降低５倍，最大反应比率分别为１．６±０．４和１．６±０．５。在去内皮的大鼠主动脉环中，经ＭＢ和Ｌ－ＮＮＡ处理后，仍可见ＥＣ３０下降３倍，最大反应比率均为１．０±０．２。后者可能与血管平滑肌产生少量ＥＤＲＦ有关。我们的结果提示ＰＥ对血管的收缩反应也受血管内皮和平滑肌产生的ＥＤＲＦ的调控
This study was to investigate the effect of EDRF (endothelium-derived protective factor) on the contractile response of aortic (PE) induced by phenylephrine in rats. Endothelial complete and endothelium-deprived rat aortic rings were suspended in organ baths and the changes in vascular tone and contractile velocity were measured. All experiments were performed in the presence of indomethacin (10 [mu] mol / L). Endothelium-intact rat aortic rings were treated with methylene blue (MB, 10 μmol / L) or L-NNA (30 μmol / L) The contractile tension curve shifted to the left significantly and the EC30 values decreased 5-fold with the maximum response rates of 1.6 ± 0.4 and 1.6 ± 0.5, respectively. In the aortic rings of endothelium-deprived rats, EC30 decreased 3-fold and the maximal response rate was 1.0 ± 0.2 after treatment with MB and L-NNA. The latter may be related to a small amount of EDRF produced by vascular smooth muscle. Our results suggest that the contractile response of PE to blood vessels is also regulated by the EDRF produced by the vascular endothelium and smooth muscle