Angiotensin-induced inflammation and novel approaches to treatment

In a brief period, we have accrued a new view of Ang II. From conventional signaling pathways, our attention was directed toward signal transduction involving specific tyrosine kinases, inducing not only vasocontriction but also proto-oncogene expression, protein synthesis, hypertrophy and growth. More recently, our attention has been directed beyond these effects to inflammatory reactions involving NF-kappa B activation and related gene expression. The mechanisms are not known for certain but probably initially involve the generation of ROS. The subsequent NF-kappa B activation probably involves participation of endothelin signaling and, perhaps, NF-AT3 activation. It is possible that other compounds can also modulate Ang II-induced inflammatory responses.