jejunum. Electrical ¢eld stimulation and applied NO (3^100 WM) evoked biphasic hyperpolarizations consisting of an
initial transient hyperpolarizing component followed by a second more slowly developing component (late component).
The NO synthase inhibitor NG-nitro-L-arginine methyl ester (200 WM) abolished the biphasic inhibitory junction potential
evoked by electrical ¢eld stimulation. The NO scavenger oxyhemoglobin (50 WM) and the guanylate cyclase inhibitor 1H-
[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ; 10 WM) abolished both components of the inhibitory junction potentials
and the NO-induced hyperpolarizations. VIP(6^28) (1 WM), which abolished VIP (3 WM)-induced hyperpolarizations, also
inhibited the late components of the inhibitory junction potentials and the NO-induced hyperpolarizations. ODQ inhibited
VIP release and cAMP production by electrical ¢eld stimulation and NO application. N6-2,0-Dibutyryladenosine
3P,5P-cyclic monophosphate (0.1^3 mM) caused a membrane hyperpolarization.
These results suggest that NO may stimulate VIP release from enteric nerves in the hamster jejunum. In addition, we
propose that NO and NO-stimulated VIP contribute to the early and late components of the inhibitory junction
potentials, respectively, in the circular smooth muscle cells of the hamster jejunum.