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Role of NADPH oxidase in the pressor and dipsogenic actions of angiotensin II in the rat brain

This study examined the role of NADPH oxidase in the central actions of Angiotensin II (Ang II). NADPH generated reactive oxygen species (ROS) have been identified as an important intracellular second messenger in a number of Ang II regulated cellular processes in the periphery. Recently, adenoviral vectors encoding a dominant‐ negative isoform of Rac1,were shown to inhibit Ang II‐induced Rac 1 dependent NADPH oxidase stimulation and Ang II induced cardiovascular and dipsogenic effects when administered into the mouse brain (Zimmerman et al., 2004). Rats were implanted with a guide cannula for intracerebroventricular (ICV) injection and a telemetric probe (Model TA11PA‐C40, DSI, Arden Hills, MN) in the abdominal aorta for blood pressure monitoring. Pressor and dipsogenic responses to Ang II (100 pmoles in 2 μl, ICV) were measured. 2 days later, rats were treated with the NADPH oxidase assembly inhibitor apocynin (2.5 nmol in 5 μl) followed 10 minutes later by Ang II (100 pmoles in 2 μl, ICV) and pressor and dipsogenic responses were measured. After an additional 2 days, rats were treated with Ang II (100 pmoles in 2 μl, ICV) and the responses again measured. Apocynin acutely reduced the pressor and dipsogenic responses to Ang II by 22.9 and 29.5 % respectively, (p<0.05). The inhibition was no longer apparent 2 days later. These results indicate that NADPH oxidase activation plays a role in transducing the effects of Ang II in the rat brain.