{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:47:24Z","timestamp":1787017644628,"version":"build-2736575974"},"reference-count":51,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:p>\n                    Secretagogue-stimulated intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals are fundamentally important for initiating the secretion of the fluid and ion component of saliva from parotid acinar cells. The Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals have characteristic spatial and temporal characteristics, which are defined by the specific properties of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release mediated by inositol 1,4,5-trisphosphate receptors (InsP\n                    <jats:sub>3<\/jats:sub>\n                    R). In this study we have investigated the role of adenine nucleotides in modulating Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release in mouse parotid acinar cells. In permeabilized cells, the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release rate induced by submaximal [InsP\n                    <jats:sub>3<\/jats:sub>\n                    ] was increased by 5 mM ATP. Enhanced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release was not observed at saturating [InsP\n                    <jats:sub>3<\/jats:sub>\n                    ]. The EC\n                    <jats:sub>50<\/jats:sub>\n                    for the augmented Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release was \u223c8 \u03bcM ATP. The effect was mimicked by nonhydrolysable ATP analogs. ADP and AMP also potentiated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release but were less potent than ATP. In acini isolated from InsP\n                    <jats:sub>3<\/jats:sub>\n                    R-2-null transgenic animals, the rate of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release was decreased under all conditions but now enhanced by ATP at all [InsP\n                    <jats:sub>3<\/jats:sub>\n                    ]. In addition the EC\n                    <jats:sub>50<\/jats:sub>\n                    for ATP potentiation increased to \u223c500 \u03bcM. These characteristics are consistent with the properties of the InsP\n                    <jats:sub>3<\/jats:sub>\n                    R-2 dominating the overall features of InsP\n                    <jats:sub>3<\/jats:sub>\n                    R-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release despite the expression of all isoforms. Finally, Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals were measured in intact parotid lobules by multiphoton microscopy. Consistent with the release data, carbachol-stimulated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals were reduced in lobules exposed to experimental hypoxia compared with control lobules only at submaximal concentrations. Adenine nucleotide modulation of InsP\n                    <jats:sub>3<\/jats:sub>\n                    R in parotid acinar cells likely contributes to the properties of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals in physiological and pathological conditions.\n                  <\/jats:p>","DOI":"10.1152\/ajpgi.00328.2011","type":"journal-article","created":{"date-parts":[[2011,9,30]],"date-time":"2011-09-30T06:46:53Z","timestamp":1317365213000},"page":"G97-G104","source":"Crossref","is-referenced-by-count":16,"title":["Regulation of Ca\n                    <sup>2+<\/sup>\n                    release through inositol 1,4,5-trisphosphate receptors by adenine nucleotides in parotid acinar cells"],"prefix":"10.1152","volume":"302","author":[{"given":"Hyung Seo","family":"Park","sequence":"first","affiliation":[{"name":"University of Rochester Medical Center, Department of Pharmacology and Physiology, University of Rochester, Rochester, New 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