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Nephrol Dial Transplant (1999) 14: 2585-2589
© 1999 European Renal Association-European Dialysis and Transplant Association

Invited Comments

Angiotensin II and oxidized LDL: an unholy alliance creating oxidative stress

Jan Galle and Kathrin Heermeier

Department of Medicine, Division of Nephrology, University Hospital of Würzburg, Würzburg, Germany

Correspondence and offprint requests to: Dr J. Galle, Dept. of Medicine, Division of Nephrology, University Hospital Würzburg, Josef-Schneider-Str. 2, D-97080 Würzburg, Germany.

General pathophysiological consequences of enhanced oxidative stress for vascular and renal function

Reactive oxygen species are produced continuously in many, not only vascular or renal, tissues and are part of the unspecific defence system. However, in various vascular or renal diseases enhanced formation of reactive oxygen species is thought to be pathogenic, e.g. in atherosclerosis, glomerular disease, renal failure, pyelonephritis or aminoglycoside nephropathy [1–4]. In the vascular system, the formation of O2- from endothelial cells, smooth muscle cells and macrophages seems to be of major relevance [3] mainly due to its reaction with nitric oxide (NO), particularly in the setting of hypercholesterolaemia and atherosclerosis [5]. NO, the most important endothelium-derived relaxing factor, is scavenged by O2- [6,7]. NO reacts with O2- to yield peroxynitrite (ONOO-), which is rather stable but can rearrange to form nitrate and the highly reactive OH• radical. Important pathophysiological consequences of enhanced oxygen radical formation . . . [Full Text of this Article]

Specific effects of Ang II and OxLDL

Evidence for enhanced oxidative stress induced by Ang II
Mechanism of Ang II-induced O2- production
Functional consequence of Ang II-induced oxidative stress
Evidence for enhanced oxidative stress induced by OxLDL
Mechanism of OxLDL-induced O2- production
Functional consequence of OxLDL-induced oxidative stress
Potential interaction between Ang II and OxLDL

Rationale for a potential interaction between Ang II and OxLDL
Co-localization of OxLDL and Ang II
Clinical studies
Receptor expression
Conclusion

Acknowledgments

Notes

References


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