There is likely to be differences, because the two cells express different enzymes capable of producing ROS. ECs in general always have Nox2, whereas SMCs are more variable. SMCs from certain vessels may not express all the subunits that characterize the Nox2 complex. SMCs on the other hand usually express Nox1 whereas ECs generally don't. Also, ECs express epoxygenases which are sources of O2-, whereas SMCs (except those of the pulmonary circulation) do not. It depends largely on the stimulus. It is also worth considering experimental approach. As stated above, ECs generally lack Nox1 but this can increase during culture process, or during hypoxia. Another example, arsenite, which activates Nox2, in ECs translates to the accumulation of ROS within minutes, whereas in SMCs this may take longer, up to 11h, to initiate because these cells may lack certain subunits. Here, arsenite evoked ROS accumulation is more linked to increasing levels of p22phox rather than acute Nox2 activation.
No problem. My JPET review on arsenic explains the implications of such variation..... well in relation to arsenic anyway. I have now uploaded the full text for this.