Background/Aims: Once a peptic ulcer has developed, angiogenesis plays a critical role in its healing by enhancing the microcirculation in the healing site. Previous reports have shown that Helicobacter pylori infection delays the healing of chronic gastric ulcers. To elucidate the mechanism of delayed ulcer healing caused by H. pylori, we investigated the expression of angiogenic growth factors and their receptors in gastric epithelial cells and vascular endothelial cells. Methods: After AGS gastric epithelial cells were infected with H. pylori, the expression of vascular endothelial growth factor(VEGF) and angiopoietin(Ang)-1/-2 mRNA and protein was assessed by RT-PCR and Western blot analysis, respectively. After human umbilical vein endothelial cells(HUVEC) were treated with H. pylori water extract(HPWE), angiogenic phenotype was determined by capillary tube formation and DNA synthesis assay. The expression of the receptors of VEGF and Ang-1/-2 was assessed by RT-PCR and Western blot analysis in HUVEC, and by double immunofluorescent staining in gastric mucosa. Angiogenic signaling in HUVEC was evaluated by using a quantitative intracellular calcium mobilization assay. Results: The expression of VEGF and Ang-1/-2 was not affected by H. pylori in AGS cells. In HUVEC, HPWE significantly inhibited capillary tube formation and DNA synthesis, and down-regulated the expression of receptors of VEGF and Ang. HPWE suppressed VEGF-induced intracellular calcium signaling in HUVEC. Conclusions: This study suggests that H. pylori inhibits the expression of angiogenic growth factor receptors in vascular endothelial cells, which could explain, in part, the delayed healing of gastric ulcer by H. pylori. (Korean J Helicobacter Res Prac 2002;2:139-147)