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Principal and intercalated cells perform different physiological tasks and exhibit distinctive morphology. However, acid\u2010secreting A\u2010 and base secreting B\u2010type of intercalated cells cannot be easily separated in functional studies. We used BCECF\u2010sensitive intracellular pH (pH\n                    <jats:sub>i<\/jats:sub>\n                    ) measurements in split\u2010opened collecting ducts followed by immunofluorescent microscopy in WT and intercalated cell\u2010specific ClC\u2010K2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice to demonstrate that ClC\u2010K2 inhibition enables to distinguish signals from A\u2010 and B\u2010intercalated cells. We show that ClC\u2010K2 Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    channel is expressed on the basolateral side of intercalated cells, where it governs Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    \u2010dependent H\n                    <jats:sup>+<\/jats:sup>\n                    \/HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    transport. ClC\u2010K2 blocker, NPPB, caused acidification or alkalization in different subpopulations of intercalated cells in WT but not ClC\u2010K2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Immunofluorescent assessment of the same collecting ducts revealed that NPPB increased pH\n                    <jats:sub>i<\/jats:sub>\n                    in AE1\u2010positive A\u2010type and decreased pH\n                    <jats:sub>i<\/jats:sub>\n                    in pendrin\u2010positive B\u2010type of intercalated cells. Induction of metabolic acidosis led to a significantly augmented abundance and H\n                    <jats:sup>+<\/jats:sup>\n                    secretion in A\u2010type and decreased proton transport in B\u2010type of intercalated cells, whereas metabolic alkalosis caused the opposite changes in intercalated cell function, but did not substantially change their relative abundance. Overall, we show that inhibition of ClC\u2010K2 can be employed to discriminate between A\u2010 and B\u2010type of intercalated cells in split\u2010opened collecting duct preparations. We further demonstrate that this method can be used to independently monitor changes in the functional status and abundance of A\u2010 and B\u2010type in response to systemic acid\/base stimuli.\n                  <\/jats:p>","DOI":"10.1096\/fj.202200160r","type":"journal-article","created":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T09:56:16Z","timestamp":1648547776000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["ClC\u2010K2 Cl\n                    <sup>\u2212<\/sup>\n                    channel allows identification of A\u2010 and B\u2010type of intercalated cells in split\u2010opened collecting ducts"],"prefix":"10.1096","volume":"36","author":[{"given":"Kyrylo","family":"Pyrshev","sequence":"first","affiliation":[{"name":"Department of Integrative Biology and Pharmacology the University of Texas Health Science Center at Houston  Houston Texas 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