Components of the angiotensin system cause release of a neutrophil chemoattractant from cultured bovine and human endothelial cells
| Autor: | H W, Farber, D M, Center, S, Rounds, S M, Danilov |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Umbilical Veins
medicine.medical_specialty Angiotensin receptor Captopril Neutrophils In Vitro Techniques Pulmonary Artery Bradykinin Renin-Angiotensin System chemistry.chemical_compound Internal medicine Renin–angiotensin system medicine Animals Humans Chemoattractant activity Aorta Cells Cultured Chromatography High Pressure Liquid Angiotensin II receptor type 1 Chemotactic Factors biology business.industry Angiotensin II Interleukin-8 Angiotensin-converting enzyme Endothelial stem cell Chemotaxis Leukocyte Endocrinology chemistry biology.protein Cattle Endothelium Vascular Angiotensin I Saralasin Cardiology and Cardiovascular Medicine business |
| Zdroj: | European Heart Journal. 11:100-107 |
| ISSN: | 1522-9645 0195-668X |
| DOI: | 10.1093/eurheartj/11.suppl_b.100 |
| Popis: | 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 simulate 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. |
| Databáze: | OpenAIRE |
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