{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:38:57Z","timestamp":1773459537035,"version":"3.50.1"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1989,9,1]],"date-time":"1989-09-01T00:00:00Z","timestamp":620611200000},"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":[[1989,9]]},"abstract":"<jats:p>1. The carotid body chemoreceptors are stimulated in situ by cyanide (CN\u2010), which mimics the effect of hypoxia. We have shown that CN\u2010 increases a calcium\u2010dependent potassium conductance (gK(Ca)) in single type I cells dissociated from the carotid body of the rabbit. We have now used the Ca2(+)\u2010sensitive fluorophore, Fura\u20102, to measure intracellular Ca2+ directly in single type I cells. 2. CN\u2010 reversibly increased [Ca2+]i from approximately 90 nM to a mean of approximately 200 nM. Some of this Ca2+ originated from an intracellular store, which was depleted by exposure to Ca2(+)\u2010free solutions. Prolonged application of CN\u2010 caused a sustained increase in [Ca2+]i, suggesting that CN\u2010 impairs the removal or sequestration of Ca2+. 3. pHi measured with the dye BCECF (2,7\u2010bis(2\u2010carboxyethyl)\u20105(and\u20106)\u2010carboxyfluorescein) did not change consistently in response to CN\u2010, although pHi changed predictably in response to both ammonium chloride and to acidification of the superfusate with CO2. 4. Potassium\u2010induced depolarization (35 mM\u2010K+) caused a large, cadmium\u2010sensitive rise in [Ca2+]i. The K(+)\u2010induced Ca2+ load was used to study the regulation of [Ca2+]i. 5. The clearance of a Ca2+ load was slowed either by removal of [Na+]o or by application of CN\u2010. This shows that both a Na+\u2010Ca2+ exchange and an energy\u2010dependent process or processes contribute to the regulation of [Ca2+]i. 6. Carbachol (CCh, 10\u2010100 microM), which also hyperpolarizes type I cells, caused a small transient rise in [Ca2+]i, indicating release from an exhaustible intracellular pool. The response to CN\u2010 was unaffected by prior or continued exposure to CCh, suggesting that the two stimuli operate by distinct mechanisms. 7. The increased gK(Ca) seen in type I cells in response to CN\u2010 thus reflects a change in cellular Ca2+ homeostasis. The rise in [Ca2+]i presumably underlies the documented increase in transmitter release from the carotid body in response to CN\u2010. If chemotransduction is a consequence of the release of transmitters from the type I cell, the response of the carotid body to CN\u2010, and possibly also to hypoxia, is thus a direct consequence of the energy dependence of Ca2+ homeostasis in the type I cell.<\/jats:p>","DOI":"10.1113\/jphysiol.1989.sp017769","type":"journal-article","created":{"date-parts":[[2014,12,18]],"date-time":"2014-12-18T23:44:17Z","timestamp":1418946257000},"page":"421-434","source":"Crossref","is-referenced-by-count":66,"title":["Measurements of intracellular Ca2+ in dissociated type I cells of the rabbit carotid body."],"prefix":"10.1113","volume":"416","author":[{"given":"T J","family":"Biscoe","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M R","family":"Duchen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D A","family":"Eisner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S C","family":"O'Neill","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Valdeolmillos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1989,9]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1989.sp017769","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1989.sp017769","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,22]],"date-time":"2023-10-22T00:48:07Z","timestamp":1697935687000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1989.sp017769"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1989,9]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1989,9]]}},"alternative-id":["10.1113\/jphysiol.1989.sp017769"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1989.sp017769","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1989,9]]}}}