D'Orleans-Juste P, Mitchell J A, Wood E G, Hecker M, Vane J R
William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London, U.K.
Can J Physiol Pharmacol. 1992 May;70(5):687-94. doi: 10.1139/y92-088.
The release of endothelium-derived relaxing factor (EDRF), prostacyclin (PGI2), and endothelin-1 (ET-1) was measured from endothelial cells (EC) cultured from either bovine vena cava (BVCEC) or bovine aorta (BAEC). EDRF release was determined by using the superfusion bioassay technique, whereas ET-1 and PGI2 were measured by specific radioimmunoassays. Bradykinin (BK) (0.05-30 pmol) given through columns of venous or arterial EC induced a dose-dependent release of EDRF. BK (0.05 pmol) evoked a release of EDRF from venous EC that was similar to the effect of a dose of 1 pmol from arterial EC. As with BAEC, infusions of NG-monomethyl-L-arginine (30 microM) caused an inhibition of EDRF release from BVCEC that was partially reversed by coinfusions of L-arginine (L-Arg; 100 microM). BK also induced a dose-dependent release of PGI2 from BVCEC. BVCEC and BAEC produced PGI2 in equivalent amounts when arachidonic acid (9.2 and 32 pmol) was added to the Krebs' solution perfusing the cells. BVCEC and BAEC released detectable amounts of ET-1 (0.4 +/- 0.1 and 0.9 +/- 0.3 ng/mL, respectively), over a 4-h period, and the release of ET-1 was increased approximately twofold by coincubations with thrombin (0.05-1 U/mL). These findings demonstrate that venous EC have a similar capacity to arterial EC to release vasoactive factors, thus supporting the hypothesis that veins have a functional endothelium that may modulate venous tone and platelet function.
从牛腔静脉（BVCEC）或牛主动脉（BAEC）培养的内皮细胞（EC）中测量内皮衍生舒张因子（EDRF）、前列环素（PGI2）和内皮素-1（ET-1）的释放。EDRF释放通过超灌流生物测定技术测定，而ET-1和PGI2通过特异性放射免疫测定法测量。通过静脉或动脉EC柱给予缓激肽（BK）（0.05 - 30 pmol）可诱导EDRF呈剂量依赖性释放。BK（0.05 pmol）引起静脉EC释放EDRF，其效果与动脉EC中1 pmol剂量的效果相似。与BAEC一样，输注NG-单甲基-L-精氨酸（30 μM）会抑制BVCEC释放EDRF，而共同输注L-精氨酸（L-Arg；100 μM）可部分逆转这种抑制作用。BK还可诱导BVCEC释放PGI2呈剂量依赖性。当向灌注细胞的Krebs溶液中添加花生四烯酸（9.2和32 pmol）时，BVCEC和BAEC产生等量的PGI2。在4小时内，BVCEC和BAEC释放出可检测量的ET-1（分别为0.4±0.1和0.9±0.3 ng/mL），并且与凝血酶（0.05 - 1 U/mL）共同孵育可使ET-1的释放增加约两倍。这些发现表明，静脉EC与动脉EC释放血管活性因子的能力相似，从而支持静脉具有功能性内皮可调节静脉张力和血小板功能这一假说。
