The study concerned the effect of ascorbate on the contractile response induced by DMPP in the guinea-pig ileal longitudinal muscle. At 0.5-10 mM, sodium ascorbate shifted the dose-response curve for DMPP to the left and enhanced the maximum contraction. On the other hand, in the presence of ascorbate, the high potassium (40 mM)-induced contraction was not altered, and the contraction by acetylcholine and histamine in concentrations higher than 1 microM and 0.3 microM, respectively, was slightly reduced. Thus, ascorbate enhanced the contractile response caused by DMPP which induced acetylcholine release from nerve terminals indirectly by stimulating the ganglia of the Auerbach's plexus elements. This potentiating effect of ascorbate was studied with a dual organ bath which was partitioned into two compartments. When the oral half of the muscle strip was directly stimulated by DMPP applied to the oral compartment, a contraction of the unstimulated anal part was observed. This contraction was blocked by atropine or adenosine applied to the unstimulated part. Tetrodotoxin, applied to the stimulated part, abolished the contraction of the unstimulated part. The contraction of the unstimulated part was enhanced by ascorbate applied to the stimulated part but not to the unstimulated part. These results indicate that the contraction observed in the unstimulated part may have been caused by acetylcholine release from cholinergic nerves as a result of conduction of the oral part excitation by DMPP along cholinergic nerve fibers; ascorbate may have affected the ganglion cells in Auerbach's plexus to potentiate the action of DMPP.