{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:28:08Z","timestamp":1761060488391},"reference-count":50,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2000,1,1]]},"abstract":"<jats:p> In many nonexcitable cells, hormones and neurotransmitters activate Na<jats:sup>+<\/jats:sup> influx and mobilize Ca<jats:sup>2+<\/jats:sup> from intracellular stores. The stores are replenished by Ca<jats:sup>2+<\/jats:sup>influx via \u201cstore-operated\u201d Ca<jats:sup>2+<\/jats:sup> channels (SOC). The main routes of Na<jats:sup>+<\/jats:sup> entry in these cells are unresolved, and no role for Na<jats:sup>+<\/jats:sup> in signaling has been recognized. We demonstrate that the SOC are a major Na<jats:sup>+<\/jats:sup> entry route in arterial myocytes. Unloading of the Ca<jats:sup>2+<\/jats:sup>stores with cyclopiazonic acid (a sarcoplasmic reticulum Ca<jats:sup>2+<\/jats:sup> pump inhibitor) and caffeine induces a large external Na<jats:sup>+<\/jats:sup>-dependent rise in the cytosolic Na<jats:sup>+<\/jats:sup> concentration. One component of this rise in cytosolic Na<jats:sup>+<\/jats:sup> concentration is likely due to Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchange; it depends on elevation of cytosolic Ca<jats:sup>2+<\/jats:sup> and is insensitive to 10 mM Mg<jats:sup>2+<\/jats:sup> and 10 \u03bcM La<jats:sup>3+<\/jats:sup>. Another component is inhibited by Mg<jats:sup>2+<\/jats:sup> and La<jats:sup>3+<\/jats:sup>, blockers of SOC; this component persists in cells preloaded with 1,2-bis(2-aminophenoxy)ethane- N, N, N\u2032, N\u2032-tetraacetic acid to buffer Ca<jats:sup>2+<\/jats:sup> transients and prevent Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchange-mediated Na<jats:sup>+<\/jats:sup> entry. This Na<jats:sup>+<\/jats:sup> entry apparently is mediated by SOC. The Na<jats:sup>+<\/jats:sup> entry influences Na<jats:sup>+<\/jats:sup> pump activity and Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchange and has unexpectedly large effects on cell-wide Ca<jats:sup>2+<\/jats:sup> signaling. The SOC pathway may be a general mechanism by which Na<jats:sup>+<\/jats:sup> participates in signaling in many types of cells. <\/jats:p>","DOI":"10.1152\/ajpcell.2000.278.1.c163","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T22:34:06Z","timestamp":1514154846000},"page":"C163-C173","source":"Crossref","is-referenced-by-count":108,"title":["Na<sup>+<\/sup> entry via store-operated channels modulates  Ca<sup>2+<\/sup>signaling in arterial myocytes"],"prefix":"10.1152","volume":"278","author":[{"given":"Assaf","family":"Arnon","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John M.","family":"Hamlyn","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mordecai P.","family":"Blaustein","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/328275a0"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/27094"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.275.5.F633"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1997.272.2.C428"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1993.264.6.C1513"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.79.5.1438"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(95)90408-5"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)35689-8"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0165-6147(94)90282-8"},{"key":"B11","doi-asserted-by":"crossref","first-page":"266","DOI":"10.1016\/S0165-6147(98)01181-X","volume":"19","author":"Gibson A.","year":"1998","journal-title":"Trends Pharmacol. 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