{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T10:23:16Z","timestamp":1784197396925,"version":"3.55.0"},"reference-count":29,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2003,6,1]],"date-time":"2003-06-01T00:00:00Z","timestamp":1054425600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2003,6]]},"abstract":"<jats:p>Using a Ca<jats:sup>2+<\/jats:sup>\u2010imaging technique, we studied the action of ATP on the intracellular Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) of fura\u20102\u2010loaded mixtures of type I and type II cells dissociated from rat carotid bodies. ATP (100 \u03bc<jats:sc>m<\/jats:sc>) triggered a transient rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> in the spindle\u2010shaped type II (sustentacular) cells, but not the ovoid type I (glomus) cells. When challenged with ionomycin (1 \u03bc<jats:sc>m<\/jats:sc>), no amperometry signal could be detected from the ATP\u2010responsive type II cells, suggesting that these cells lacked catecholamine\u2010containing granules. In contrast, KCl depolarization triggered robust quantal catecholamine release from type I cells that were not responsive to ATP. In type II cells voltage clamped at \u221270 mV, the ATP\u2010induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> rise was not accompanied by any current change, suggesting that P2X receptors are not involved. The ATP\u2010induced Ca<jats:sup>2+<\/jats:sup> signal could be observed in the presence of Ni<jats:sup>2+<\/jats:sup> (a blocker of voltage\u2010gated Ca<jats:sup>2+<\/jats:sup> channels) or in the absence of extracellular Ca<jats:sup>2+<\/jats:sup>, indicating that Ca<jats:sup>2+<\/jats:sup> release from intracellular stores was the dominant mechanism. The order of purinoreceptor agonist potency in triggering the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> rise was UTP &gt; ATP &gt; 2\u2010methylthioATP \u226b\u03b1,\u03b2\u2010methyleneATP, implicating the involvement of P2Y<jats:sub>2<\/jats:sub> receptors. In carotid body sections, immunofluorescence revealed localization of P2Y<jats:sub>2<\/jats:sub> receptors on spindle\u2010shaped type II cells that partially enveloped ovoid type I cells. Since ATP is released from type I cells during hypoxia, we suggest that the ATP\u2010induced Ca<jats:sup>2+<\/jats:sup> signal in type II cells can mediate paracrine interactions within the carotid bodies.<\/jats:p>","DOI":"10.1113\/jphysiol.2003.039735","type":"journal-article","created":{"date-parts":[[2003,5,6]],"date-time":"2003-05-06T00:16:14Z","timestamp":1052180174000},"page":"739-747","source":"Crossref","is-referenced-by-count":72,"title":["ATP Triggers Intracellular Ca<sup>2+<\/sup> Release in Type II Cells of the Rat Carotid Body"],"prefix":"10.1113","volume":"549","author":[{"given":"Jianhua","family":"Xu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederick 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