Responses of salivary acinar cells to intracellular alkalinization

Responses of rat submandibular acini to intracellular alkalinization were investigated. Intracellular alkalinization was induced by addition of NH 4 Cl or methylamines, or by prepulse with Na butyrate. Only partial recovery occurred following Na butyrate prepulse or methylated amine addition, but full recovery was observed following addition of NH 4 Cl. The latter recovery was DIDS and dimethylamiloride‐insensitive but was inhibited by bumetanide or high [K + ] and stimulated in Na + free buffer and by ouabain. Acetylcholine stimulated recovery from NH 4 Cl‐ or Na butyrate pre‐pulse‐induced alkalinization and reduced the extent of alkalinization induced by methylated amines. Acetylcholine‐stimulated recovery from NH 4 Cl‐induced alkalinization was mimicked by substance P or ionomycin and was partially Ca 2+ ‐dependent. This stimulated recovery was bumetanide‐insensitive but was partially sensitive to charybdotoxin. Taken together, these data indicate that in unstimulated cells, recovery from alkalinization induced by NH 4 Cl occurs by bumetanide‐sensitive transport of the NH 4+ ion, that DIDS‐inhibitable anion transport contributes little to this recovery, and that acetylcholine and other Ca 2+ ‐elevating agents accelerate recovery from NH 4 Cl‐induced alkaline challenge by a mechanism insensitive to bumetanide, DIDS, ouabain, and dimethylamiloride but sensitive to extracellular Ca 2+ and to charybdotoxin. Partial recovery from alkaline challenge can also occur in the absence of NH 4+ ions, and acetylcholine also stimulates this mode of recovery. Together, these data suggest that these cells have little intrinsic ability to recover from intracellular alkalinization and that the NH 4+ ion may be a surrogate for K + in at least two ion transport pathways. © 1994 wiley‐Liss, Inc.