The influence of nitric oxide (NO) on the spontaneous tone and on the
contractile responses to electrical field stimulation or to exogenous
acetylcholine (ACh) was studied. Circular strips from the guinea-pig g
astric fundus were used. The NO-releasing compound sodium nitroprussid
e reduced the spontaneous tone while the NO-synthase inhibitor N-G-nit
ro-L-arginine methyl ester (L-NAME) increased it. The L-NAME-induced i
ncrease of the tone was antagonized by atropine or indomethacin, sugge
sting the involvement of cholinergic and prostaglandinergic pathways i
n this effect. L-NAME significantly potentiated the ACh (10(-8) to 10(
-5) M)-induced contractions. L-NAME concentration-dependently potentia
ted the cholinergic contractions evoked by electrical field stimulatio
n without affecting [H-3]ACh overflow from [H-3]choline-treated tissue
s. It is concluded that electrical field stimulation of gastric fundus
muscle induces the release of endogenous nitrate which, in turn, func
tionally antagonizes cholinergic neurotransmission.