Intercalated cell-specific Rh B glycoprotein deletion diminishes renal ammonia excretion response to hypokalemia

Jesse M. Bishop, Hyun Wook Lee, Mary E. Handlogten, Ki Hwan Han, Jill W. Verlander, I. David Weiner

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

The ammonia transporter family member, Rh B Glycoprotein (Rhbg), is an ammoniaspecific transporter heavily expressed in the kidney and is necessary for the normal increase in ammonia excretion in response to metabolic acidosis. Hypokalemia is a common clinical condition in which there is increased renal ammonia excretion despite the absence of metabolic acidosis. The purpose of this study was to examine Rhbg's role in this response through the use of mice with intercalated cell-specific Rhbg deletion (IC-Rhbg-KO). Hypokalemia induced by feeding a K+-free diet increased urinary ammonia excretion significantly. In mice with intact Rhbg expression, hypokalemia increased Rhbg protein expression in intercalated cells in the cortical collecting duct (CCD) and in the outer medullary collecting duct (OMCD). Deletion of Rhbg from intercalated cells inhibited hypokalemia-induced changes in urinary total ammonia excretion significantly and completely prevented hypokalemia- induced increases in urinary ammonia concentration, but did not alter urinary pH. We conclude that hypokalemia increases Rhbg expression in intercalated cells in the cortex and outer medulla and that intercalated cell Rhbg expression is necessary for the normal increase in renal ammonia excretion in response to hypokalemia.

Original languageEnglish
Pages (from-to)F422-F431
JournalAmerican Journal of Physiology - Renal Physiology
Volume304
Issue number4
DOIs
StatePublished - 15 Feb 2013

Keywords

  • Acid-base
  • Ammonia
  • Collecting duct
  • Potassium
  • Rhbg

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