Abstract
Several nonsteroidal anti-inflammatory drugs (NSAIDs) were tested for their action on the Cl−/HCO3 − exchange by antiports and on the regulation of cytosolic pH (pHi) in Vero cells. The Na+-independent Cl−/HCO3 − antiport restores cytosolic pH (pHi) to normal after alkalinisation of the cytosol, and is therefore in a state of high activity at alkaline pHi, whereas it is in a state of low activity when pHi is below neutral. Preincubation with presumably anti-inflammatory concentrations of aspirin (acetylsalicylic acid), salicyclic acid, indomethacin or piroxicam at pH < 7 strongly increased the activity of this antiport, producing a decrease in pHi. Higher doses of the drugs competitively inhibited the Na+-independent Cl−/HCO3 − antiport. The Na+-coupled Cl−/HCO3 − antiport, which is most active when the pHi is < 7 and which normalises pHi after acidification, was inhibited after preincubation with these drugs, both at therapeutic and at higher concentrations. Preincubation with the drugs reduced pHi by 0.05 to 0.4 pH units compared with that in cells incubated in the absence of drugs.
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