Signaling Pathways Involved in Renal Oxidative Injury: Role of the Vasoactive Peptides and the Renal Dopaminergic System

Figure 3

Effects of ANP on NOS activity in the kidney. NO synthesis can be stimulated by ANP via NPRA receptors. It has also been reported that NPRC natriuretic receptor mediates the activation of NOS by ANP. This evidence is in accordance with studies supporting a protective role of ANP against oxidative stress. In contrast, there is evidence indicating that ANP inhibits the inducible nitric oxide synthase (iNOS) activity via NPRC, leading to the increase of NO levels. It has been shown that an increment in renal NOS activity together with ROS production (represented as superoxide anion ) is able to increase cytotoxic peroxynitrites (ONOO⁻) which in turn reduce NO bioavailability, leading to oxidative stress. The mechanisms by which ANP regulates NOS activity in the kidney are not completely elucidated (blue arrow: stimulatory effect, red arrow: inhibitory effect, question mark: contradictory evidence supporting both stimulatory and inhibitory effects of ANP on NOS activity, and PDE: phosphodiesterase).