Abstract
We have recently shown that Rac-1 mediated-NOX2 release of O2− has a permissive effect on epithelial sodium channel (ENaC) activity. The objective of this study was to determine whether changes in single channel ENaC recordings indeed translate into significant changes in lung fluid clearance. Using a novel fluoroscopic assay for measuring lung fluid volume in vivo, we showed that NSC23766 inhibition of Rac1 in 3 month old C57Bl6 mice significantly decreased fluid clearance (n=7) compared to untreated control animals (n=10). Similarly, fluid challenged gp91phox −/− knock out mice (−/−Cybb; n=7) failed to clear lung fluid compared to age matched control (n=8). We also show for the first time that inhibition of Rac1 decreases the oxidative state of the lung using novel redox sensitive hydrocyanine compounds (n=3). In conclusion, our results indicate that targeting small G protein Rac1 and NOX2 production of O2− may be a useful therapeutic for treating several various lung disorders.
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