Figure 3.

NADPH oxidase is functionally disrupted in the lungs of CGD mice. (A) Isolated lungs from CGD mice produce less AOS than wild-type mice, whether measured unenhanced or with lucigenin (∗, P < 0.05). PMA increases lucigenin chemiluminescence in lungs from wild-type, but not CGD, mice (†, P < 0.05). (B) Lucigenin-enhanced chemiluminescence is diminished by acute hypoxia and by DPI in rat PA rings (fourth division) denuded of endothelium. ∗, P < 0.05 value differs from normoxia. (C) Schematic of two competing theories for redox regulation of K⁺ channels. In one, a gp91 phox containing NADPH produces AOS, which modulate channel function through effects on critical channel cysteine groups. In the other, inhibition of mitochondrial complex 1 leads to accumulation of cytosolic reducing equivalents, which in turn inhibit the K⁺ channel by interaction with its cysteine groups.