Omeprazole induces gastric transmucosal permeability to the peptide bradykinin.

To investigate omeprazole-induced transepithelial gastric leak and its effects on the permeability of the peptides bradykinin and oxytocin. Rat gastric corpus tissue was isolated and mounted in an Ussing chamber apparatus to evaluate the permeability of (3)H-bradykinin, (3)H-oxytocin, and (14)C-EDTA in the presence or absence of omeprazole. Thin-layer chromatography was performed to identify any metabolic breakdown products of the peptides resulting from permeation through the gastric tissue, and thereby calculate the true flux of the peptide. The flux rate of intact (3)H-bradykinin increased substantially after omeprazole addition (109.5%) compared to the DMSO vehicle control (14%). No corresponding change in flux of intact (3)H-oxytocin was observed under the same conditions (11.9% and 6.4% in the DMSO- and omeprazole-treated conditions, respectively). After exposure to omeprazole, the flux rate of (14)C-EDTA also increased dramatically (122.3%) compared to the DMSO condition (36.3%). The omeprazole-induced gastric leak allows for transmucosal permeability to charged molecules as well as non-electrolytes. This induced leak will allow certain peptides to permeate.