ClC-K2 Cl- channel allows identification of A- and B-type of intercalated cells in split-opened collecting ducts

FASEB J. 2022 May;36(5):e22275. doi: 10.1096/fj.202200160R.

Abstract

The collecting duct is a highly adaptive terminal part of the nephron, which is essential for maintaining systemic homeostasis. Principal and intercalated cells perform different physiological tasks and exhibit distinctive morphology. However, acid-secreting A- and base secreting B-type of intercalated cells cannot be easily separated in functional studies. We used BCECF-sensitive intracellular pH (pHi ) measurements in split-opened collecting ducts followed by immunofluorescent microscopy in WT and intercalated cell-specific ClC-K2-/- mice to demonstrate that ClC-K2 inhibition enables to distinguish signals from A- and B-intercalated cells. We show that ClC-K2 Cl- channel is expressed on the basolateral side of intercalated cells, where it governs Cl- -dependent H+ /HCO3- transport. ClC-K2 blocker, NPPB, caused acidification or alkalization in different subpopulations of intercalated cells in WT but not ClC-K2-/- mice. Immunofluorescent assessment of the same collecting ducts revealed that NPPB increased pHi in AE1-positive A-type and decreased pHi in pendrin-positive B-type of intercalated cells. Induction of metabolic acidosis led to a significantly augmented abundance and H+ secretion in A-type and decreased proton transport in B-type 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-K2 can be employed to discriminate between A- and B-type of intercalated cells in split-opened collecting duct preparations. We further demonstrate that this method can be used to independently monitor changes in the functional status and abundance of A- and B-type in response to systemic acid/base stimuli.

Keywords: AE1; V-ATPase; acid-base disorders; intracellular pH; pendrin.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Acidosis* / metabolism
  • Animals
  • Anion Transport Proteins / genetics
  • Anion Transport Proteins / metabolism
  • Kidney Tubules, Collecting* / metabolism
  • Mice
  • Nephrons / metabolism
  • Sulfate Transporters / metabolism

Substances

  • Anion Transport Proteins
  • Sulfate Transporters