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

Title
Intercalated cell-specific Rh B glycoprotein deletion diminishes renal ammonia excretion response to hypokalemia
Authors
Bishop J.M.Lee H.-W.Handlogten M.E.Han K.-H.Verlander J.W.David Weiner I.
Ewha Authors
한기환
SCOPUS Author ID
한기환scopus
Issue Date
2013
Journal Title
American Journal of Physiology - Renal Physiology
ISSN
0363-6127JCR Link
Citation
vol. 304, no. 4, pp. F422 - F431
Indexed
SCOPUS WOS scopus
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. Copyright © 2013 the American Physiological Society.
DOI
10.1152/ajprenal.00301.2012
Appears in Collections:
의과대학 > 의학과 > Journal papers
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