{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T09:21:27Z","timestamp":1789809687325,"version":"4.0.1"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1994,7,1]],"date-time":"1994-07-01T00:00:00Z","timestamp":773020800000},"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":[[1994,7]]},"abstract":"<jats:p>1. An acid\u2010induced rise in the intracellular calcium concentration ([Ca2+]i) of type I cells is thought to play a vital role in pH\/PCO2 chemoreception by the carotid body. In this present study we have investigated the cause of this rise in [Ca2+]i in enzymatically isolated, neonatal rat type I cells. 2. The rise in [Ca2+]i induced by a hypercapnic acidosis was inhibited in Ca(2+)\u2010free media, and by 2 mM Ni2+. Acidosis also increased Mn2+ permeability. The rise in [Ca2+]i is dependent, therefore, upon a Ca2+ influx from the external medium. 3. The acid\u2010induced rise in [Ca2+]i was attenuated by both nicardipine and methoxyverapamil (D600), suggesting a role for L\u2010type Ca2+ channels. 4. Acidosis depolarized type I cells and often (approximately 50% of cells) induced action potentials. These effects coincided with a rise in [Ca2+]i. When membrane depolarization was prevented by a voltage clamp, acidosis failed to evoke a rise in [Ca2+]i. The acid\u2010induced rise in [Ca2+]i is a consequence, therefore, of membrane depolarization. 5. Acidosis decreased the resting membrane conductance of type I cells. The reversal potential of the acid\u2010sensitive current was about \u201075 mV. 6. A depolarization (30 mM [K+]o)\u2010induced rise in [Ca2+]i was blocked by either the removal of extracellular Ca2+ or the presence of 2 mM Ni2+, and was also substantially inhibited by nicardipine. Under voltage\u2010clamp conditions, [Ca2+]i displayed a bell\u2010shaped dependence on membrane potential. Depolarization raises [Ca2+]i, therefore, through voltage\u2010operated Ca2+ channels. 7. Caffeine (10 mM) induced only a small rise in [Ca2+]i (&lt; 10% of that induced by 30 mM extracellular K+). Ca(2+)\u2010induced Ca2+ release is unlikely, therefore, to contribute greatly to the rise in [Ca2+]i induced by depolarization. 8. Although the replacement of extracellular Na+ with N\u2010methyl\u2010D\u2010glucamine (NMG), but not Li+, inhibited the acid\u2010induced rise in [Ca2+]i, this was due to membrane hyperpolarization and not to the inhibition of Na(+)\u2010Ca2+ exchange or Na(+)\u2010dependent action potentials. 9. The removal of extracellular Na+ (NMG substituted) did not have a significant effect upon the resting [Ca2+]i, and only slowed [Ca2+]i recovery slightly following repolarization from 0 to \u201060 mV. Therefore, if present, Na(+)\u2010Ca2+ exchange plays only a minor role in [Ca2+]i homeostasis. 10. In summary, in the neonatal rat type I cell, hypercapnic acidosis raises [Ca2+]i through membrane depolarization and voltage\u2010gated Ca2+ entry.<\/jats:p>","DOI":"10.1113\/jphysiol.1994.sp020239","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T12:15:36Z","timestamp":1418818536000},"page":"157-171","source":"Crossref","is-referenced-by-count":123,"title":["Effects of hypercapnia on membrane potential and intracellular calcium in rat carotid body type I cells."],"prefix":"10.1113","volume":"478","author":[{"given":"K J","family":"Buckler","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R D","family":"Vaughan-Jones","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1994,7]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1994.sp020239","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1994.sp020239","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T12:23:07Z","timestamp":1698150187000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1994.sp020239"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,7]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1994,7]]}},"alternative-id":["10.1113\/jphysiol.1994.sp020239"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1994.sp020239","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,7]]}}}