Figure 3.

Importance of free radical production by immune cells in the development of salt-sensitive (SS) hypertension and renal end-organ damage. (a) The development of SS hypertension and albuminuria (as a surrogate for renal damage) is attenuated in Dahl SS rats with a whole body null mutation in the p67phox subunit of NOX2 (SS^{p67phox−/−}). (b) Total body irradiation of SS^{p67phox−/−} followed by bone marrow transfer from SS or SS^{p67phox−/−} demonstrated that intact p67phox (and thus active NOX2) in cells of hematopoietic origin is sufficient to restore the full SS disease phenotype to SS rats lacking p67phox in parenchymal cells. *P < 0.05, **P < 0.005, ***P < 0.001 vs. SS. Redrawn from Abais-Battad et al.¹³⁵ with permission.