Kim J A, Berliner J A, Nadler J L
Department of Diabetes & Endocrinology, City of Hope Medical Center, Duarte, CA 91010, USA.
Biochem Biophys Res Commun. 1996 Sep 24;226(3):862-8. doi: 10.1006/bbrc.1996.1441.
Angiotensin II (AII) is recognized as being an important factor in the pathogenesis of hypertension and atherosclerosis. Monocyte binding to affected endothelial cells is one of the earliest features of atherosclerosis. However, the effect of AII on monocyte binding has not been fully studied. Treatment of human aortic endothelial cells (HAEC) and rabbit aortic endothelial cells (RAEC) for 18 hours with AII induced the adhesion of monocytes but not neutrophils to these cells. This induction was reduced by inhibitors of AII receptors (Type I and Type II). Angiotensin II-induced monocyte binding was not associated with induction of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), or intercellular adhesion molecule-1 (ICAM-1). These results suggest that AII can accelerate the rate of atherosclerosis by increasing monocyte binding to the endothelium.
血管紧张素II（AII）被认为是高血压和动脉粥样硬化发病机制中的一个重要因素。单核细胞与受影响的内皮细胞结合是动脉粥样硬化最早出现的特征之一。然而，AII对单核细胞结合的影响尚未得到充分研究。用AII处理人主动脉内皮细胞（HAEC）和兔主动脉内皮细胞（RAEC）18小时，可诱导单核细胞而非中性粒细胞黏附于这些细胞。AII受体（I型和II型）抑制剂可减少这种诱导作用。血管紧张素II诱导的单核细胞结合与E-选择素、血管细胞黏附分子-1（VCAM-1）或细胞间黏附分子-1（ICAM-1）的诱导无关。这些结果表明，AII可通过增加单核细胞与内皮的结合来加速动脉粥样硬化的进程。
