{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T16:46:04Z","timestamp":1759682764878},"reference-count":32,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,2,4]],"date-time":"2005-02-04T00:00:00Z","timestamp":1107475200000},"content-version":"vor","delay-in-days":3901,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[1994,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Responses of rat submandibular acini to intracellular alkalinization were investigated. Intracellular alkalinization was induced by addition of NH<jats:sup>4<\/jats:sup>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<jats:sup>4<\/jats:sup>Cl. The latter recovery was DIDS and dimethylamiloride\u2010insensitive but was inhibited by bumetanide or high [K<jats:sup>+<\/jats:sup>] and stimulated in Na<jats:sup>+<\/jats:sup> free buffer and by ouabain. Acetylcholine stimulated recovery from NH<jats:sup>4<\/jats:sup>Cl\u2010 or Na butyrate pre\u2010pulse\u2010induced alkalinization and reduced the extent of alkalinization induced by methylated amines. Acetylcholine\u2010stimulated recovery from NH<jats:sup>4<\/jats:sup>Cl\u2010induced alkalinization was mimicked by substance P or ionomycin and was partially Ca<jats:sup>2+<\/jats:sup>\u2010dependent. This stimulated recovery was bumetanide\u2010insensitive but was partially sensitive to charybdotoxin. Taken together, these data indicate that in unstimulated cells, recovery from alkalinization induced by NH<jats:sup>4<\/jats:sup>Cl occurs by bumetanide\u2010sensitive transport of the NH<jats:sup>4+<\/jats:sup> ion, that DIDS\u2010inhibitable anion transport contributes little to this recovery, and that acetylcholine and other Ca<jats:sup>2+<\/jats:sup>\u2010elevating agents accelerate recovery from NH<jats:sup>4<\/jats:sup>Cl\u2010induced alkaline challenge by a mechanism insensitive to bumetanide, DIDS, ouabain, and dimethylamiloride but sensitive to extracellular Ca<jats:sup>2+<\/jats:sup> and to charybdotoxin. Partial recovery from alkaline challenge can also occur in the absence of NH<jats:sup>4+<\/jats:sup> 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<jats:sup>4+<\/jats:sup> ion may be a surrogate for K<jats:sup>+<\/jats:sup> in at least two ion transport pathways. \u00a9 1994 wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.1041590310","type":"journal-article","created":{"date-parts":[[2005,2,26]],"date-time":"2005-02-26T04:45:05Z","timestamp":1109393105000},"page":"457-467","source":"Crossref","is-referenced-by-count":4,"title":["Responses of salivary acinar cells to intracellular alkalinization"],"prefix":"10.1002","volume":"159","author":[{"given":"Jc.","family":"Seagrave","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Curry","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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