Endothelial NOS deficiency preserves DDAH activity and attenuates the LPS induced increase in ADMA in the mouse lung.

<p>Immunoblot analysis demonstrated that LPS did not change DDAH I (A) or DDAH II (B) protein levels in the lungs of either wild-type or eNOS^-/- mice. DDAH activity, estimated by the conversion of L-[³H]-NMMA to [³H]-L-citrulline, was significantly decreased by LPS exposure in the lungs of wild-type mice (C); however, DDAH activity was not attenuated in the lungs of LPS treated eNOS^-/- mice (C). In addition, eNOS^-/- mice exhibited increased lung DDAH activity compared to wild-type mice (C). LPS exposure increased ADMA levels in wild-type mouse lungs but not in the lungs of eNOS^-/- mice (D). Values are mean ± SEM, n = 6–10. *p<0.05 vs. Wild-type+Vehicle, †P<0.05 vs. Wild-type+LPS.