NO levels (Figs. 6D and E), and augmented NO production was effectively inhibited by L-NAME, similar to the findings in flap vessels or in rat renal endothelial membrane compartments [42,43]. We also detected two other iNOS-immunoreactive bands (molecular weights of 135 and 200 kDa) both significantly up-regulated by EtOH/Ach exposure but to a lesser extent than 10-kDa species (data not shown). These results suggested that exposure of human neurons with alcohol- or Ach-induced iNOS activity led to enhance production of NO in the CNS.
