{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T16:28:58Z","timestamp":1789662538481,"version":"4.0.1"},"reference-count":60,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2017,3,20]],"date-time":"2017-03-20T00:00:00Z","timestamp":1489968000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2018,3]]},"abstract":"<jats:p>\n                    The CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    buffer minimizes pH changes in response to acid\u2013base loads, HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    provides substrate for Na\n                    <jats:sup>+<\/jats:sup>\n                    ,HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    -cotransporters and Cl\n                    <jats:sup>\u2013<\/jats:sup>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    -exchangers, and H\n                    <jats:sup>+<\/jats:sup>\n                    and HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    modify vasomotor responses during acid\u2013base disturbances. We show here that rat middle cerebral arteries express cytosolic, mitochondrial, extracellular, and secreted carbonic anhydrase isoforms that catalyze equilibration of the CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    buffer. Switching from CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    -free to CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    -containing extracellular solution results in initial intracellular acidification due to hydration of CO\n                    <jats:sub>2<\/jats:sub>\n                    followed by gradual alkalinization due to cellular HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    uptake. Carbonic anhydrase inhibition decelerates the initial acidification and attenuates the associated transient vasoconstriction without affecting intracellular pH or artery tone at steady-state. Na\n                    <jats:sup>+<\/jats:sup>\n                    ,HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    -cotransport and Na\n                    <jats:sup>+<\/jats:sup>\n                    \/H\n                    <jats:sup>+<\/jats:sup>\n                    -exchange activity after NH\n                    <jats:sub>4<\/jats:sub>\n                    <jats:sup>+<\/jats:sup>\n                    -prepulse-induced intracellular acidification are unaffected by carbonic anhydrase inhibition. Extracellular surface pH transients induced by transmembrane NH\n                    <jats:sub>3<\/jats:sub>\n                    flux are evident under CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    -free conditions but absent when the buffer capacity and apparent H\n                    <jats:sup>+<\/jats:sup>\n                    mobility increase in the presence of CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    even after the inhibition of carbonic anhydrases. We conclude that (a) intracellular carbonic anhydrase activity accentuates pH transients and vasoconstriction in response to acute elevations of pCO\n                    <jats:sub>2<\/jats:sub>\n                    , (b) CO\n                    <jats:sub>2<\/jats:sub>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2013<\/jats:sup>\n                    minimizes extracellular surface pH transients without requiring carbonic anhydrase activity, and (c) carbonic anhydrases are not rate limiting for acid\u2013base transport across cell membranes during recovery from intracellular acidification.\n                  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