The Cl−HCO3− exchanger slows the recovery of acute pHi changes in rat mast cells

Abstract The CO 2 /HCO 3 − buffering system is one of the main mechanisms implicated in cytosolic pH (pH i ) regulation. We studied this pH i -regulatory system in rat mast cells using a fluorescent dye. Mast cells had a more alkaline pH i in the presence of HCO 3 − than in its absence. The recovery from an acid load was faster in HCO 3 − -free conditions than in HCO 3 − -containing media. In HCO 3 − -buffered conditions the increase of the recovery rate of an acidification in 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid-incubated cells suggested the implication of a Na + -independent Cl − /HCO 3 − exchanger. This HCO 3 − transport acidified the cytosol and was also partially responsible for the recovery of intracellular alkalinizations. Moreover, regulation of the recovery rate of an acidification by protein kinase C and calcium signaling pathways depended on the presence or absence of HCO 3 − . The presence of HCO 3 − limits the recovery of acute intracellular acidifications probably through the Na + -independent Cl − /HCO 3 − exchanger and modulates the regulation of pH i by protein kinase C and calcium.