Nephrol Dial Transplant (2000) 15: 561-565
© 2000 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
ACE inhibitors and AT1 receptor antagonists—beyond the haemodynamic effect
Renal Unit, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain
Introduction
The classical view of angiotensin II (Ang II) as a vasoactive agent that participates in local and systemic haemodynamic regulation has been recently enlarged to consider it as a true cytokine with an active role in renal and cardiovascular pathology (reviewed in [1,2]). In several models of kidney damage, the blockade of Ang II actions by angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor antagonists ameliorates proteinuria, inflammatory cell infiltration and fibrosis [3–6]. In addition, several authors, including ourselves, have demonstrated that Ang II is a renal growth factor that modulates cell growth and extracellular matrix production [1,2,,7,,8]. Moreover, Ang II participates in the inflammatory response in the kidney through the synthesis of chemotactic factors [9]. Finally, recent studies suggested that angiotensin peptides other than Ang II are bioactive agents with potential implication in renal
Action of Ang II on cell growth and matrix synthesis
Ang II and mononuclear cell recruitment
Angiotensin receptors and inflammation
Ang II and nuclear factor-
B
New aspects of the RAS. The Ang II degradation products
Acknowledgments
Notes
References
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