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European Heart Journal 1990 11(Supplement B):100-107; doi:10.1093/eurheartj/11.suppl_B.100
Copyright © 1990 by the European Society of Cardiology.
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© 1990 The European Society of Cardiology

Components of the angiotensin system cause release of a neutrophil chemoattractant from cultured bovine and human endothelial cells

H. W. Farber, D. M. Center, S. Rounds and S. M. Danilov*

Pulmonary Center, Boston University School of Medicine Boston, Massachusetts, U.S.A.
* Institute of Experimental Cardiology, USSR Cardiology Research Center Moscow, USSR

Correspondence and reprint requests to: Harrison W. Farber, MD, Pulmonary Center, Boston University School of Medicine, 80 East Concord Street, Boston, MA 02118, U.S.A.

Evidence suggests that angiotensin II can affect macrophage-mediated inflammatory responses; however, whether it can affect neutrophil-mediated inflammatory responses is not yet clear. We have previously demonstrated that components of the angiotensin system stimulate bovine aortic and human umbilical vein endothelial cells to release a neutrophil chemoattractant. In the current study, we examined the effect of components of the angiotensin system on bovine and human pulmonary arterial and human aortic endothelial cells, and partially characterized this neutrophil chemoattractant. All endothelial cell types incubated with angiotensin II released neutrophil chemoattractant activity. This activity appeared within 1 min of exposure to angiotensin II, and was blocked by saralasin, an angiotensin II antagonist. The neutrophil chemoattractant also appeared after exposure to angiotensin I, but this effect required conversion to angiotensin II. Incubation with bradykinin, another substrate for angiotensin-converting enzyme, did not cause release of the neutrophil chemoattractant. Chemoattractant release was not inhibited by indomethacin but was blocked by diethylcarbamazine or 5,8,11,14-eicosatetraynoic acid. Following extraction, the neutrophil chemoattractant partitioned completely into the organic phase. High-pressure liquid chromatography demonstrated several peaks of chemoactivity, none of which co-eluted with known eicosanoid or phospholipid neutrophil chemoattractants. This study demonstrates that angiotensin II may influence neutrophil accumulation via production of neutrophil chemoattractant activity by vascular endothelial cells.

Key Words: Endothelial cells • angiotensin II • chemotaxis • neutrophil migration


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