{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T18:52:42Z","timestamp":1785178362499,"version":"3.55.0"},"reference-count":34,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1998,8,1]]},"abstract":"<jats:p> This study examines the Ca<jats:sup>2+<\/jats:sup> influx-dependent regulation of the Ca<jats:sup>2+<\/jats:sup>-activated K<jats:sup>+<\/jats:sup> channel (K<jats:sub>Ca<\/jats:sub>) in human submandibular gland (HSG) cells. Carbachol (CCh) induced sustained increases in the K<jats:sub>Ca<\/jats:sub> current and cytosolic Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), which were prevented by loading cells with 1,2-bis(2-aminophenoxy)ethane- N, N, N\u2032, N\u2032-tetraacetic acid (BAPTA). Removal of extracellular Ca<jats:sup>2+<\/jats:sup> and addition of La<jats:sup>3+<\/jats:sup> or Gd<jats:sup>3+<\/jats:sup>, but not Zn<jats:sup>2+<\/jats:sup>, inhibited the increases in K<jats:sub>Ca<\/jats:sub> current and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. Ca<jats:sup>2+<\/jats:sup> influx during refill (i.e., addition of Ca<jats:sup>2+<\/jats:sup> to cells treated with CCh and then atropine in Ca<jats:sup>2+<\/jats:sup>-free medium) failed to evoke increases in the K<jats:sub>Ca<\/jats:sub> current but achieved internal Ca<jats:sup>2+<\/jats:sup> store refill. When refill was prevented by thapsigargin, Ca<jats:sup>2+<\/jats:sup> readdition induced rapid activation of K<jats:sub>Ca<\/jats:sub>. These data provide further evidence that intracellular Ca<jats:sup>2+<\/jats:sup> accumulation provides tight buffering of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>at the site of Ca<jats:sup>2+<\/jats:sup> influx (H. Mogami, K. Nakano, A. V. Tepikin, and O. H. Petersen. Cell 88: 49\u201355, 1997). We suggest that the Ca<jats:sup>2+<\/jats:sup> influx-dependent regulation of the sustained K<jats:sub>Ca<\/jats:sub>current in CCh-stimulated HSG cells is mediated by the uptake of Ca<jats:sup>2+<\/jats:sup> into the internal Ca<jats:sup>2+<\/jats:sup> store and release via the inositol 1,4,5-trisphosphate-sensitive channel. <\/jats:p>","DOI":"10.1152\/ajpcell.1998.275.2.c571","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T17:49:58Z","timestamp":1514137798000},"page":"C571-C580","source":"Crossref","is-referenced-by-count":38,"title":["Regulation of K<sub>Ca<\/sub>current by store-operated Ca<sup>2+<\/sup>influx depends on internal Ca<sup>2+<\/sup>release in HSG cells"],"prefix":"10.1152","volume":"275","author":[{"given":"Xibao","family":"Liu","sequence":"first","affiliation":[{"name":"Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, 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