Gastric ulcer (GU) and duodenal ulcer (DU) occur as a result of the imbalance between aggressive and defensive factors affecting the gastroduodenal mucosa. Prostaglandins (PG) of E and I series are generated throughout the gastrointestinal tract, particularly in the gastric and duodenal mucosa, and are released into the gut lumen upon vagal and hormonal stimulation. Endogenous PGs may be involved in the maintenance of mucosal integrity, control of mucosal blood flow and protection against potentially noxious agents. Gastric mucosa of ulcer patients tends to generate smaller amounts of PGs of E and I series and exhibits a reduced ratio of PG to thromboxane generation, which suggests that the deficiency of protective PG may play a role in the pathogenesis of peptic ulcer. Suppression of mucosal generation of PGs by non-steroidal anti-inflammatory compounds causes mucosal damage and increases the risk of the formation or exacerbation of peptic ulcer. Exogenous PGE and its stable analogs have been tested successfully in the treatment of GU and DU and the results so far obtained indicate that these agents significantly increase the ulcer healing rate. Certain anti-ulcer drugs such as carbenoxolone, sucralfate, colloidal bismuth and cimetidine appear to exert their beneficial effects on ulcer healing by mediating the release of endogenous PGs.