Farber H W, Center D M, Rounds S
Circ Res. 1985 Dec;57(6):898-902. doi: 10.1161/01.res.57.6.898.
Although there is growing evidence that angiotensin II affects macrophage-mediated inflammatory responses, it is unclear whether it can affect neutrophil-mediated inflammatory responses. Because vascular endothelial cells are capable of releasing neutrophil chemoattractant activity, we attempted to determine whether components of the angiotensin system could affect neutrophil-mediated responses indirectly by stimulating endothelial cells to release neutrophil chemoattractant substances. Cultured bovine and human endothelial cells incubated with angiotensin II released neutrophil chemoattractant activity. This activity appeared within 1 minute of exposure to angiotensin II, and was blocked by saralasin, an angiotensin II antagonist. Angiotensin I also caused release of neutrophil chemoattractant activity, but its effect required conversion to angiotensin II. Bradykinin, another substrate for angiotensin-converting enzyme, did not stimulate appearance of chemoattractant. Chemoattractant generation was not inhibited by indomethacin but was blocked by diethylcarbamazine and 5,8,11,14-eicosatetraynoic acid. This study demonstrates that angiotensin II may influence neutrophil accumulation, via production of neutrophil chemoattractant activity by vascular endothelial cells.
尽管越来越多的证据表明血管紧张素II会影响巨噬细胞介导的炎症反应，但尚不清楚它是否会影响中性粒细胞介导的炎症反应。由于血管内皮细胞能够释放中性粒细胞趋化活性，我们试图确定血管紧张素系统的成分是否能通过刺激内皮细胞释放中性粒细胞趋化物质来间接影响中性粒细胞介导的反应。用血管紧张素II孵育的培养牛和人内皮细胞释放出中性粒细胞趋化活性。这种活性在接触血管紧张素II后1分钟内出现，并被血管紧张素II拮抗剂沙拉新阻断。血管紧张素I也会引起中性粒细胞趋化活性的释放，但其作用需要转化为血管紧张素II。缓激肽是血管紧张素转换酶的另一种底物，不会刺激趋化剂的出现。趋化剂的产生不受吲哚美辛抑制，但被二乙氨基甲嗪和5,8,11,14-二十碳四烯酸阻断。这项研究表明，血管紧张素II可能通过血管内皮细胞产生中性粒细胞趋化活性来影响中性粒细胞的聚集。
