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AIM: The effect of ethacrynic acid on pancreaticexocrine secretion function and potential mechanisms ofinterference with the secreory process in pancreatic acinarcells were investigated. METHODS: After incubationwith ethacrynic acid for 30 min, caerulein-stimulatedamylase release and cholecystokinin (CCK) receptorbinding characteristics were assessed in isolated ratpancreatic acini. The level of thiol groups (glutathioneand protein thiols) and cytosolic free calcium weremeasured in pancreatic acinar cells. RESULTS:Ethacynic acid decreased caerulein (0. 1 nmol/L)-stimulated amylase release and the level of pancreaticacinar glutathione in a concentration-dependent fashionwithout a marked increase in cell damage. Ethacrynicacid also inhibited the caerulein (1 nmol/L)-inducedCa~(2+) mobilization in pancreatic acinar cells. But neitherprotein thiol nor CCK-receptor binding characteristics wasaltered by ethacrynic acid. CONCLUSION: Ethacrynicacid inhibit pancreatic exocrine secretion by depletion ofglutathion
AIM: The effect of ethacrynic acid on pancreatic xocrine secretion function and potential mechanisms of interference with the secreory process in pancreatic acinar cells were investigated. METHODS: After incubation with ethacrynic acid for 30 min, caerulein-stimulated amylase release and cholecystokinin (CCK) receptor binding were were in assessed in The levels of thiol groups (glutathione and protein thiols) and cytosolic free calcium were measured in pancreatic acinar cells. RESULTS: Ethacynic acid decreased caerulein (0.1 nmol / L) -stimulated amylase release and the level of pancreatic acid in glutathione in a concentration -dependent fashionwithout a marked increase in cell damage. Ethacrynicacid also inhibited the caerulein (1 nmol / L) -inducedCa ~ (2) mobilization in pancreatic acinar cells. But neither protein endocytosis wasaltered by ethacrynic acid. CONCLUSION: Ethacrynicacid inhibit pancreatic exocrine secretion by depl etion ofglutathion