Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
2996169
Reference Type
Journal Article
Subtype
Review
Title
Ammonia transport in the kidney by Rhesus glycoproteins
Author(s)
Weiner, ID; Verlander, JW
Year
2014
Is Peer Reviewed?
Yes
Journal
American Journal of Physiology: Renal Physiology
ISSN:
1931-857X
Volume
306
Issue
10
Page Numbers
F1107-F1120
Language
English
PMID
24647713
DOI
10.1152/ajprenal.00013.2014
Web of Science Id
WOS:000336846400001
URL
http://ajprenal.physiology.org/content/306/10/F1107
Exit
Abstract
Renal ammonia metabolism is a fundamental element of acid-base homeostasis, comprising a major component of both basal and physiologically altered renal net acid excretion. Over the past several years, a fundamental change in our understanding of the mechanisms of renal epithelial cell ammonia transport has occurred, replacing the previous model which was based upon diffusion equilibrium for NH3 and trapping of NH4(+) with a new model in which specific and regulated transport of both NH3 and NH4(+) across renal epithelial cell membranes via specific membrane proteins is required for normal ammonia metabolism. A major advance has been the recognition that members of a recently recognized transporter family, the Rhesus glycoprotein family, mediate critical roles in renal and extrarenal ammonia transport. The erythroid-specific Rhesus glycoprotein, Rh A Glycoprotein (Rhag), was the first Rhesus glycoprotein recognized as an ammonia-specific transporter. Subsequently, the nonerythroid Rh glycoproteins, Rh B Glycoprotein (Rhbg) and Rh C Glycoprotein (Rhcg), were cloned and identified as ammonia transporters. They are expressed in specific cell populations and membrane domains in distal renal epithelial cells, where they facilitate ammonia secretion. In this review, we discuss the distribution of Rhbg and Rhcg in the kidney, the regulation of their expression and activity in physiological disturbances, the effects of genetic deletion on renal ammonia metabolism, and the molecular mechanisms of Rh glycoprotein-mediated ammonia transport.
Keywords
acid-base; ammonia; collecting duct; intercalated cell; principal cell
Tags
IRIS
•
Ammonia
Literature Search Update – Sept 2015 (private)
Literature Search Results
Cited 2016
ToxReview
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity