RESPONSES OF SALIVARY ACINAR-CELLS TO INTRACELLULAR ALKALINIZATION

Responses of rat submandibular acini to intracellular alkalinization w ere investigated. Intracellular alkalinization was induced by addition of NH4Cl or methyl amines, or by prepulse with Na butyrate. Only part ial recovery occurred following Na butyrate prepulse or methylated ami ne addition, but full recovery was observed following addition of NH4C l. The latter recovery was DIDS and dimethylamiloride-insensitive but was inhibited by bumetanide or high [K+] and stimulated in Na+-free bu ffer and by ouabain. Acetylcholine stimulated recovery from NH4Cl- or Na butyrate pre-pulse-induced alkalinization and reduced the extent of alkalinization induced by methylated amines. Acetylcholine-stimulated recovery from NH4Cl-induced alkalinization was mimicked by substance P or ionomycin and was partially Ca2+-dependent. This stimulated recov ery was bumetanide-insensitive but was partially sensitive to charybdo toxin. Taken together, these data indicate that in unstimulated cells, recovery from alkalinization induced by NH4Cl occurs by bumetanide-se nsitive transport of the NH4+ ion, that DIDS-inhibitable anion transpo rt contributes little to this recovery, and that acetylcholine and oth er Ca2+-elevating agents accelerate recovery from NH4Cl-induced alkali ne challenge by a mechanism insensitive to bumetanide, DIDS, ouabain, and dimethylamiloride but sensitive to extracellular Ca2+ and to chary bdotoxin. Partial recovery from alkaline challenge can also occur in t he absence of NH4+ ions, and acetylcholine also stimulates this mode o f recovery. Together, these data suggest that these cells have little intrinsic ability to recover from intracellular alkalinization and tha t the NH4+ ion may be a surrogate for K+ in at least two ion transport pathways. (C) 1994 Wiley-Liss, Inc.