[The renin-angiotensin system and post-ischemic angiogenesis]

This article summarizes the main mechanisms responsible for the ischemia-induced neovascularization. Growth factors and inflammatory agents are the most powerful actors in the neo-vascularization process. Numerous other factors have been shown to modulate blood vessel growth. Among these, we have tested the potential effect of angiotensin II in several in vivo models of angiogenesis. Angiotensin II has pro-angiogenic effects via its AT1 subtype receptor whereas the AT2 angiotensin II receptor has pro-apoptotic and anti-angiogenic properties. Besides its effect on angiotensin II formation, some angiotensin-converting-enzyme inhibitors have pro-angiogenic effect by increasing the local concentration of bradykinin in ischemic tissues and, thus, by activation of its B2 receptor and then NO release. These besides the "classical" gene and cellular therapies designed for the treatment of pathological tissue ischemia, alternative strategies using new pharmacological properties of drugs acting on the renin angiotensin system are likely to be possible.