The pathogenesis of linear ulceration induced by restraint water-immersion (RWI) was investigated in view of gastric motility and early ischemic changes. After three hours of restraint-water immersion stress, the cross-sectioned gastric body was prepared for light microscopy. Most lesions (90.8%) were present in the mucosal folds projecting toward the cavity. Wedge-shaped degeneration in the crest of the folds was recognized as an ischemic lesion followed by hemorrhagic ulceration. Compressed arterioles were frequently encountered in the muscularis mucosae and circular muscle. Generally, mucosal folds appear merely with the reduction of gastric content, and run along with the elevation of the circular muscle as an anatomical structure, becoming tall and steep after RWI. Marked enhancement of contraction, observed with a strain gauge force transducer, was induced by RWI. This enhancement was suppressed by papaverine HCl pretreatment in accordance with suppression of the fold-related mucosal lesion even after 150 mM HCl perfusion into the stomach. In conclusion, gastric motility appears to play an important role in the pathogenesis of linear ulceration by causing ischemic change along the folds.