Mechanism of action of aspirin on canine gastric mucosa.
Using an in vivo chambered canine stomach preparation, exposure of the gastric mucosa to 5, 10, and 20 mM aspirin(pH 3.0) resulted in a decrease in electrical potential difference (PD) and in an increase in resistance (R) within 30 min. In vitro, exposure of the mucosal side of the isolated canine gastric mucosa to 5, 10, and 20 mM aspirin (pH 3.0) for 1 h or of 1 mM aspirin (pH 3.0) for longer than 1 h resulted in marked permeability changes, i.e., increases in the undirectional fluxes of Na+ and Cl-, as well as inhibition of net ion fluxes. These concentrations of nonionized aspirin (pH 3.0) also reduced the R and PD. However, 1 mM aspirin (pH 3.0) or 20 mM ionized aspirin (pH 7.4) depresses the active transport of ion, increases R, but does not increase the ionic permeability. Mucosal adenosine triphosphate (ATP) content is reduced by mucosal instillation of aspirin (pH 3.0). These results demonstrate that the initial action of aspirin is inhibition of ion transport which is followed by an increase in permeability.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001693:Biological Transport, Active / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004594:Electrophysiology; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D010539:Permeability; D012964:Sodium / Q000378:metabolism
D002712:Chlorides; D012964:Sodium; D001241:Aspirin