In human radial arteries, a nitric oxide/prostanoid- independent mechanism
that has the pharmacological characteristics of an EDHF contributes to endo
thelium- dependent relaxation. H2O2 can act as an EDHF in some vascular bed
s. We examined the hypothesis that endogenously produced H2O2 mediated the
nitric oxide/ prostanoid-independent relaxation to carbachol in radial arte
ries obtained from patients undergoing coronary artery bypass surgery. Supe
roxide levels, measured by chemiluminescence, were similar in radial and in
ternal mammary arteries, but immunohistochemical staining for Cu/Zn superox
ide dismutase (SOD) was lower in endothelium from radial arteries. In organ
chamber studies, neither addition of catalase nor addition of SOD to the b
athing fluid modified nitric oxide/prostanoid- independent relaxations to c
arbachol in radial arteries. However, nitric oxide-dependent vasorelaxation
was enhanced in the presence of SOD. Thus the nitric oxide/ prostanoid-ind
ependent relaxation to carbachol is not due to H2O2 and, unlike nitric oxid
e-mediated vasorelaxation, is not attenuated by superoxide. Blood vessels s
howing EDHF-mediated relaxations resistant to oxidative stress may provide
favorable outcomes in revascularization surgery.