Document Detail

New insights into urinary acidification and regulation of acid-base balance.
MedLine Citation:
PMID:  21510485     Owner:  NLM     Status:  In-Process    
Systemic acid-base balance is primarily controlled by the renal excretion of acids and the exhalation of CO2 and both processes are tightly regulated and coordinated. Acid excretion into urine requires the formation of ammonium and its transport into urine as gaseous ammonia. Until recently it has been believed that NH3 would move across membranes by free diffusion according to Overton's rule. Recent structural, functional, and in vivo data show now that Rhesus proteins act as gas channels for NH3 and mediate renal acid excretion. Lack of the renal isoform RhCG in mice causes reduced ammonium excretion and metabolic acidosis. Breathing and exhalation of CO2 is stimulated and regulated by CO2 and acid sensors in the carotid bodies and the brain stem. GPR4 belongs to a small subfamily of G protein-coupled receptors and is activated by extracellular protons. Mice lacking GPR4 develop respiratory acidosis and are not able to increase ventilation appropriately in response to high CO2 levels or systemic acidosis. Thus, RhCG and GPR4 present novel paradigms of membrane proteins involved in controlling and regulating systemic acid-base balance in the major organs involved in this task.
C Wagner
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Bulletin et mémoires de l'Académie royale de médecine de Belgique     Volume:  165     ISSN:  0377-8231     ISO Abbreviation:  Bull. Mem. Acad. R. Med. Belg.     Publication Date:  2010  
Date Detail:
Created Date:  2011-04-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7608462     Medline TA:  Bull Mem Acad R Med Belg     Country:  Belgium    
Other Details:
Languages:  eng     Pagination:  259-64; discussion 265-6     Citation Subset:  IM    
Institute of Physiology, University of Zurich, Switzerland.
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