['Endothelin-1, a key mediator of inflammatory processes, is produced from its biologically inactive precursor, big ET- by the action of endothelin converting enzyme-1(ECE-1). In this study, we applied the animal model of H. pylori lipopolysaccharide-induced gastritis to assess the effect of three different types of antiulcer agents on the gastric mucosal expression of ECE-1 activity.', 'Rats, pretreated twice daily for 3 days with proton pump inhibitor, omeprazole at 40 mg/kg, gastroprotective agent, sulglycotide at 200 mg/kg, H2-receptor antagonist, ebrotidine at 100 mg/kg or the vehicle, were subjected to intragastric application of H. pylori lipopolysaccharide at 50 microg/animal, and after 2, and 4 additional days on the drug or vehicle regimen their mucosal tissue used for histologic and biochemical assessment.', 'In the absence of antiulcer agents, H. pylori lipopolysaccharide elicited a pattern of mucosal inflammatory responses resembling that of acute gastritis which reached a maximum by the 4th day and were accompanied by a 4.1-fold increase in the mucosal expression of ECE-1 activity and an 8.8-fold enhancement in TNF-alpha. Treatment with sulglycotide led to a 56.7% reduction in the extent of mucosal inflammatory involvement, the mucosal expression of ECE-1 activity fell by a 40.5% and the level of TNF-alpha declined by a 69%. Ebrotidine produced a 50.9% decrease in the extent of mucosal inflammatory involvement, a 33.6% decrease in the expression of ECE-1 activity and a 64.1% decline in TNF-alpha, whereas omeprazole elicited a 37.6% reduction in the extent of mucosal inflammatory involvement and a 29.5% decrease in TNF-alpha, but had no effect on the lipoploysaccharide-induced increase in the mucosal expression of ECE-1 activity.'] Does omeprazole fail to suppress up-regulation of gastric mucosal endothelin-converting enzyme-1 by Helicobacter pylori lipopolysaccharide?