The role of nitric oxide (NO) in the development of allergic cutaneous
reactions in mice was investigated. A biphasic cutaneous reaction com
posed of an immediate-phase edema and a late-phase edema was evoked by
epicutaneous application of 2,4-dinitrofluorobenzene on the ear of mi
ce passively sensitized with mouse anti-dinitrophenol monoclonal IgE.
Two NO synthase inhibitors, L-N-G-nitroarginine methyl ester (L-NAME)
and N-G-monomethyl-L-arginine, significantly inhibited both phases of
the IgE-mediated biphasic cutaneous reaction. Simultaneous treatment w
ith L-arginine attenuated the inhibitory effect oft-NAME. An NO donor,
3-morpholinosydononimine-N-ethylcarbamide, caused a potent edematous
reaction in the mouse ear. Furthermore, L-NAME inhibited the cutaneous
reactions caused by both interleukin-1 beta and tumor necrosis factor
-alpha, putative mediators of the late-phase edema in the biphasic cut
aneous reaction. These results indicate that a gaseous mediator, NO, p
articipates, at least in part, in the development of ear edema in the
IgE-mediated biphasic cutaneous reaction in mice.