{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T12:59:17Z","timestamp":1791118757214,"version":"4.1.0"},"reference-count":0,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[1994,9,1]],"date-time":"1994-09-01T00:00:00Z","timestamp":778377600000},"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":[[1994,9]]},"abstract":"<jats:p>1. HCO3(\u2010)\u2010dependent mechanisms involved in the regulation of intracellular pH (pHi) were characterized using double\u2010barrelled pH\u2010sensitive microelectrodes in smooth muscle cells of the isolated guinea\u2010pig ureter. 2. Removal of external Cl\u2010 in the presence of CO2\u2010HCO3\u2010 caused a transient alkalosis, consistent with the presence of Cl(\u2010)\u2010HCO3\u2010 exchange, before pHi slowly recovered. Recovery from acidosis in the presence of CO2\u2010HCO3\u2010 was not affected, at a time when intracellular Cl\u2010 would have been maximally depleted, indicating that a counter transport of Cl\u2010 and HCO3\u2010 was not involved. The recovery was also not affected by amiloride, indicating that Na(+)\u2010H+ exchange was not involved. 3. A transient hyperpolarization was associated with the recovery from acidosis in the presence of CO2\u2010HCO3\u2010, consistent with rheogenic coupling of Na(+)\u2010HCO3\u2010 cotransport. However, depolarization caused by elevation of the extracellular potassium (K+o) concentration, which should favour inward transport by the rheogenic mechanism, caused a fall in pHi and decreased the rate of recovery from acidosis. Furthermore, ouabain abolished the transient hyperpolarization without affecting the recovery of pHi. It is concluded that Na(+)\u2010HCO3\u2010 cotransport in the ureter is electroneutral. 4. Recovery from acidosis in the presence of CO2\u2010HCO3\u2010 was insensitive to DIDS even after prolonged pre\u2010equilibriation and extreme acidosis. The results suggest that Na(+)\u2010HCO3\u2010 cotransport in the ureter is insensitive to DIDS and that Cl(\u2010)\u2010HCO3\u2010 exchange does not reverse to contribute to the extrusion of acid equivalents. A HCO3\u2010 conductance may account for the Na(+)\u2010independent, HCO3(\u2010)\u2010dependent recovery from extreme acidosis. 5. Recovery from experimentally induced alkalosis was inhibited by Cl(\u2010)\u2010free conditions and by DIDS, indicating that Cl(\u2010)\u2010HCO3\u2010 exchange was involved. 6. It is concluded that pHi in the smooth muscle of guinea\u2010pig ureter is controlled by three transport mechanisms. By far the most important is an electroneutral Na(+)\u2010HCO3\u2010 cotransporter. Na(+)\u2010H+ exchange appears to play little role in the presence of the physiological buffer. Both of these mechanisms extrude acid equivalents and so protect the cell against its fairly substantial intrinsic intracellular acid loading. Cl(\u2010)\u2010HCO3\u2010 exchange, on the other hand, is stimulated by intracellular alkalosis to transport acid equivalents into the cell and so restore a more normal pHi.<\/jats:p>","DOI":"10.1113\/jphysiol.1994.sp020298","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T12:04:39Z","timestamp":1418817879000},"page":"317-329","source":"Crossref","is-referenced-by-count":18,"title":["Regulation of intracellular pH in the smooth muscle of guinea\u2010pig ureter: HCO3\u2010 dependence."],"prefix":"10.1113","volume":"479","author":[{"given":"C C","family":"Aickin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1994,9]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1994.sp020298","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1994.sp020298","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T12:43:59Z","timestamp":1698151439000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1994.sp020298"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,9]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1994,9]]}},"alternative-id":["10.1113\/jphysiol.1994.sp020298"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1994.sp020298","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,9]]}}}