AE anion exchangers in atrial tumor cells

Intracellular pH homeostasis and intracellular Cl- concentration in cardiac myocytes are regulated by anion exchange mechanisms. In physiological extr acellular Cl- concentrations, Cl-/HCO3- exchange promotes intracellular aci dification and Cl- loading sensitive to inhibition by stilbene disulfonates . We investigated the expression of AE anion exchangers in the AT-1 mouse a trial tumor cell line. Cultured AT-1 cells exhibited a substantial basal Na +-independent Cl-/HCO3- (but not Cl-/OH-) exchange activity that was inhibi ted by DIDS but not by dibenzamidostilbene disulfonic acid (DBDS). AT-1 cel l Cl-/HCO3- activity was stimulated two- to threefold by extracellular ATP and ANG II. AE mRNAs detected by RT-PCR in AT-1 cells included brain AE3 (b AE3), cardiac AE3 (cAE3), AE2a, AE2b, AE2c1, AE2c2, and erythroid AE1 (eAE1 ), but not kidney AE1 (kAE1). Cultured AT-1 cells expressed AE2, cAE3, and bAE3 polypeptides, which were detected by immunoblot and immunocytochemistr y. An AE1-like epitope was detected by immunocytochemistry but not by immun oblot. Both bAE3 and cAE3 were present in intact AT-1 tumors. Cultured AT-1 cells provide a useful system for the study of mediators and regulators of Cl-/HCO3- exchange activity in an atrial cell type.