Kelm M, Feelisch M, Spahr R, Piper H M, Noack E, Schrader J
Zentrum für Physiologie und Klin, Physiologie, Universität Düsseldorf, FRG.
Biochem Biophys Res Commun. 1988 Jul 15;154(1):236-44. doi: 10.1016/0006-291x(88)90675-4.
Endothelial cells (EC) contribute to the control of local vascular diameter by formation of an endothelium derived relaxant factor (EDRF) (1). Whether nitric oxide (NO) is identical with (EDRF) or might represent only one species of several EDRFs has not been decided as yet (2-5). Therefore, we have directly compared in cultured EC the kinetics of NO formation determined in a photometric assay with the vasodilatory effect of EDRF and NO in a bioassay. Basal release of NO was 16, 4 pmol/min/ml packed EC column. After stimulation with bradykinin (BK) and ATP onset of endothelial NO release and maximal response preceded the EDRF-mediated relaxation. Concentrations of NO formed by stimulated EC were quantitatively sufficient to fully explain the smooth muscle relaxation determined in the bioassay. Our data provide convincing evidence that under basal, BK and ATP-stimulated conditions 1. endothelial cells release nitric oxide as free radical, 2. nitric oxide is solely responsible for the vasodilatory properties of EDRF.
内皮细胞(EC)通过形成一种内皮衍生舒张因子(EDRF)来控制局部血管直径(1)。一氧化氮(NO)是否与EDRF相同,或者是否仅代表几种EDRF中的一种,目前尚未确定(2 - 5)。因此,我们在培养的内皮细胞中,直接比较了光度测定法测定的NO生成动力学与生物测定法中EDRF和NO的血管舒张作用。NO的基础释放量为16.4 pmol/分钟/毫升填充内皮细胞柱。用缓激肽(BK)和ATP刺激后,内皮NO释放的起始和最大反应先于EDRF介导的舒张。受刺激的内皮细胞形成的NO浓度在数量上足以充分解释生物测定中确定的平滑肌舒张。我们的数据提供了令人信服的证据,即在基础、BK和ATP刺激条件下:1. 内皮细胞释放作为自由基的一氧化氮;2. 一氧化氮是EDRF血管舒张特性的唯一原因。