The renin-angiotensin system (RAS) has emerged as one of the essential links in the pathophysiology of
vascular disease.
Angiotensin (Ang) II, the main
peptide of the RAS, was considered as a vasoactive
hormone, but in the past years, this view has been modified to a
growth factor that regulates cell proliferation/apoptosis and
fibrosis. Recently, this view has been enlarged with a novel concept: Ang II participates in the inflammatory response, acting as a proinflammatory mediator. In resident vascular cells, Ang II produces
chemokines,
cytokines, and adhesion molecules, which contribute to the migration of inflammatory cells into the tissue injury. Ang II is also a chemotactic and mitogenic factor for mononuclear cells. The molecular mechanisms of Ang II-induced vascular damage are mediated by the activation of
transcription factors, redox signaling systems, and production of endogenous
growth factors. In addition, other components of the RAS could also be involved in the pathogenesis of
cardiovascular diseases. The Ang II degradation product Ang III shares some of its properties with Ang II, including chemotaxis and production of
growth factors and
chemokines. All these data clearly demonstrate that Ang II is a true
cytokine, show the complexity of the RAS in
pathological processes, and provide some mechanistic responses of the beneficial effects of the treatment with RAS blockers in
cardiovascular diseases.