{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T21:07:06Z","timestamp":1767992826536,"version":"3.49.0"},"reference-count":60,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2013,10,1]]},"abstract":"<jats:p> Chronic hypoxia (CHox) augments chemoafferent activity in sensory fibers innervating carotid body (CB) chemoreceptor type I cells; however, the underlying mechanisms are poorly understood. We tested the hypothesis that enhanced paracrine signaling via adenosine (Ado) A<jats:sub>2b<\/jats:sub> receptors is involved. Dissociated rat CB cultures were exposed for 24 h to normoxia (Nox, 21% O<jats:sub>2<\/jats:sub>) or CHox (2% O<jats:sub>2<\/jats:sub>) or treated with the hypoxia mimetic deferoxamine mesylate (DFX), and catecholamine secretion from type I cells was monitored by amperometry. Catecholamine secretion was more robust in CHox and DFX type I cells than Nox controls after acute exposure to acid hypercapnia (10% CO<jats:sub>2<\/jats:sub>, pH 7.1) and high K<jats:sup>+<\/jats:sup> (75 mM). Exogenous Ado increased catecholamine secretion in a dose-dependent manner, and the EC<jats:sub>50<\/jats:sub> was shifted to the right from \u223c21 \u03bcM Ado in Nox cells to \u223c78 \u03bcM in CHox cells. Ado-evoked secretion in Nox and CHox cells was markedly inhibited by MRS-1754, an A<jats:sub>2b<\/jats:sub> receptor blocker, but was unaffected by SCH-58261, an A<jats:sub>2a<\/jats:sub> receptor blocker. Similarly, MRS-1754, but not SCH-58261, partially inhibited high-K<jats:sup>+<\/jats:sup>-evoked catecholamine secretion, suggesting a contribution from paracrine activation of A<jats:sub>2b<\/jats:sub> receptors by endogenous Ado. CB chemostimuli, acid hypercapnia, and hypoxia elicited a MRS-1754-sensitive rise in intracellular Ca<jats:sup>2+<\/jats:sup> that was more robust in CHox and DFX than Nox cells. Taken together, these data suggest that paracrine Ado A<jats:sub>2b<\/jats:sub> receptor signaling contributes to stimulus-evoked catecholamine secretion in Nox and CHox CB chemoreceptors; however, the effects of Ado are more robust after CHox. <\/jats:p>","DOI":"10.1152\/ajpcell.00137.2013","type":"journal-article","created":{"date-parts":[[2013,7,25]],"date-time":"2013-07-25T15:00:41Z","timestamp":1374764441000},"page":"C739-C750","source":"Crossref","is-referenced-by-count":18,"title":["Enhanced adenosine A<sub>2b<\/sub> receptor signaling facilitates stimulus-induced catecholamine secretion in chronically hypoxic carotid body type I cells"],"prefix":"10.1152","volume":"305","author":[{"given":"Simon","family":"Livermore","sequence":"first","affiliation":[{"name":"Department of Biology, McMaster University, Hamilton, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Colin A.","family":"Nurse","sequence":"additional","affiliation":[{"name":"Department 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