fluid secretion by 71.7 % (p<O.05), epithelial cell damage by 56%, (p<O.05), mucosal congestion and edema by 26% (p<O.O5), and neutrophil infiltration by 60.8%, (p<O.O01). None of the CRH antagonists had any effect on basal fluid secretion. Conclusions: CRH plays a significant proinflammatory role in TxAinduced intestinal secretion and inflammation and the CRH receptor 1, at least in part, participates in the mediation of these responses. These findings may be important in the treatment of gut inflammation in view of the recent development of CRH receptor antagonists. Supported by the Crohn's and Colitis Foundation of America, Inc., and the National Institutes of Hea~th (DK 33506).