{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,15]],"date-time":"2024-09-15T05:52:41Z","timestamp":1726379561465},"reference-count":0,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[1994,4,15]],"date-time":"1994-04-15T00:00:00Z","timestamp":766368000000},"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":[[1994,4,15]]},"abstract":"<jats:p>The release of prostaglandin E2 (PGE2) from rabbit carotid bodies (CBs) incubated in basal conditions (PO2 approximately 132 mmHg; PCO2 approximately 33 mmHg; pH = 7.42) amounts to 94.4 +\/\u2010 10.1 pg (mg protein)\u20101 (10 min)\u20101 (mean +\/\u2010 S.E.M.). Incubation of the CB in a hypoxic solution (PO2 approximately 46 mmHg) produced a significant 40% increase (P &lt; 0.05) in the release of PGE2. Indomethacin (2 microM) prevented the hypoxia\u2010induced release of PGE2. Sensory plus sympathetic denervation of the CB 4 days prior to the experiments did not modify either basal or low PO2\u2010induced PGE2 release, indicating that intraglomic nerve endings are not significant sources for the PGE2 released. Incubation of the CB in an acidic\u2010hypercapnic solution (PO2 approximately 132 mmHg; PCO2 approximately 132 mmHg; pH = 6.60) or in a high K(+)\u2010containing solution (35 mM) was also effective in promoting an increase in the outflow of PGE2 from the organs. The release of [3H]catecholamines ([3H]CA) from the CB elicited by incubating the organs in low PO2 solutions (PO2 ranged between 66 and 13 mmHg) was potentiated by two inhibitors of cyclo\u2010oxygenase, acetylsalicylic acid (ASA, 100 microM) and indomethacin (2 microM). The effect persisted after chronic denervation of the organ. The secretory response elicited by acidic stimuli was also augmented by cyclo\u2010oxygenase inhibitors. Thus, [3H]CA release elicited by incubating the CBs in the acidic\u2010hypercapnic solution increased by 300% in the presence of indomethacin (2 microM), and ASA (100 microM) more than doubled the release induced by dinitrophenol (100 microM), a protonophore that mimics an acidic stimulus. Indomethacin, but not ASA, moderately increased the high K(+)\u2010evoked [3H]CA release. The effect of indomethacin on the release of [3H]CA elicited by acidic and hypoxic stimuli was reversed by PGE2 in a dose\u2010dependent manner (0.3\u2010300 nM). These results show that low PO2 and high PCO2\u2010low pH, the natural stimuli to the CB, as well as high extracellular [K+], activate the cyclo\u2010oxygenase pathway in the CB, promoting an increase in the outflow of PGE2. The data also show that the blockade of this pathway activates the stimulus\u2010induced [3H]CA release from the CB, indicating that naturally released prostanoids exert an inhibitory control on chemoreceptor cells. The data lend support to the notion that the hyper\u2010reactivity of the ventilatory response to hypoxia in subjects under anti\u2010inflammatory drug treatment results from CB cycloxygenase inhibition.<\/jats:p>","DOI":"10.1113\/jphysiol.1994.sp020128","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T12:45:15Z","timestamp":1418820315000},"page":"257-267","source":"Crossref","is-referenced-by-count":16,"title":["In vitro activation of cyclo\u2010oxygenase in the rabbit carotid body: effect of its blockade on [3H]catecholamine release."],"prefix":"10.1113","volume":"476","author":[{"given":"A","family":"G\u00f3mez\u2010Ni\u00f1o","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L","family":"Almaraz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C","family":"Gonz\u00e1lez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1994,4,15]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1994.sp020128","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1994.sp020128","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T01:05:50Z","timestamp":1698109550000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1994.sp020128"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,4,15]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1994,4,15]]}},"alternative-id":["10.1113\/jphysiol.1994.sp020128"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1994.sp020128","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,4,15]]}}}