Reactive oxygen species (ROS) are important intra-neuronal signaling intermediates in angiotensin II (AngII)-related neuro-cardiovascular diseases associated with excessive sympathoexcitation, including hypertension and heart failure. ROS-sensitive effector mechanisms, such as modulation of ion channel activity, indicate that elevated levels of ROS increase neuronal activity. Nitric oxide, which may work to counter the effects of ROS, particularly superoxide, has been identified as a signaling molecule in angiotensin-1-7 (Ang-(1-7)) stimulated neurons. This review focuses on recent studies that have revealed details on the AngII-activated sources of ROS, the downstream redox-sensitive effectors, Ang-(1-7)-stimulated increase in nitric oxide, and the neuro-cardiovascular (patho)physiological responses modulated by these reactive species. Understanding these intra-neuronal signaling mechanisms should provide insight for the development of new redox-based therapeutics for the improved treatment of angiotensin-dependent neuro-cardiovascular diseases.
ASJC Scopus subject areas
- Drug Discovery