Weber C, Kruse H J, Sellmayer A, Erl W, Weber P C
Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten University of Munich, Germany.
Biochem Biophys Res Commun. 1993 Sep 15;195(2):874-80. doi: 10.1006/bbrc.1993.2126.
Platelet activating factor (PAF) primes vascular actions of mediators such as histamine and stimulates human umbilical vein endothelial cells (HUVECs) to produce prostacyclin (PGI2), which is important for the regulation of vascular tone, perfusion and hemostasis. We demonstrate that pretreatment of HUVECs with PAF enhances thrombin- or histamine-induced rises of cytosolic free Ca(++)-concentration and subsequent Ca(++)-dependent PGI2-synthesis. Inhibition of Ca(++)-influx and PGI2-formation by SKF96365 (blocker of receptor-operated Ca(++)-channels) in PAF-treated cells indicates that the enhancement of PGI2-synthesis by PAF is due to sensitization of Ca(++)-entry. This suggests cooperative effects of PAF on activation processes induced by thrombin or histamine in HUVECs.
血小板活化因子（PAF）可引发组胺等介质的血管作用，并刺激人脐静脉内皮细胞（HUVECs）产生前列环素（PGI2），这对于调节血管张力、灌注和止血至关重要。我们证明，用PAF预处理HUVECs可增强凝血酶或组胺诱导的胞质游离Ca（++）浓度升高以及随后的Ca（++）依赖性PGI2合成。在PAF处理的细胞中，SKF96365（受体操纵性Ca（++）通道阻滞剂）对Ca（++）内流和PGI2形成的抑制表明，PAF对PGI2合成的增强是由于Ca（++）内流的致敏作用。这表明PAF对HUVECs中凝血酶或组胺诱导的激活过程具有协同作用。
