Document Detail

Angiotensin II receptors mediate increased distal nephron acidification caused by acid retention.
MedLine Citation:
PMID:  22832514     Owner:  NLM     Status:  MEDLINE    
Patients with a moderately reduced glomerular filtration rate (GFR) typically have no metabolic acidosis and a urine net acid excretion comparable to those with normal GFR, supporting greater per nephron acidification with moderately reduced GFR. We modeled such patients using rats with a surgical reduction of 2/3 kidney mass, yielding animals with reduced GFR without metabolic acidosis. We then tested the hypothesis that reduction of nephron mass augments distal nephron acidification in remnant nephrons mediated by increased angiotensin II activity, and that the latter is induced by underlying acid retention. Nephron mass reduction yielded lower GFR than controls (sham operation), higher acid retention (measured by microdialysis of kidney cortex), higher distal nephron acidification, and higher plasma and kidney levels of angiotensin II, but plasma total CO(2) and urine net acid excretion were not different. Angiotensin II receptor antagonism reduced distal nephron acidification to levels similar to control. Dietary alkali that lowered acid retention to that of control also reduced plasma and kidney levels of angiotensin II and reduced distal nephron acidification to control. Angiotensin II receptor antagonism with dietary alkali had no significant added effect on distal nephron acidification. Thus, nephron reduction that moderately reduced GFR with no metabolic acidosis is characterized by increased angiotensin II activity. This mediates increased distal nephron acidification and is induced by acid retention.
Donald E Wesson; Chan-Hee Jo; Jan Simoni
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-07-25
Journal Detail:
Title:  Kidney international     Volume:  82     ISSN:  1523-1755     ISO Abbreviation:  Kidney Int.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-15     Completed Date:  2013-04-29     Revised Date:  2013-07-19    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1184-94     Citation Subset:  IM    
Texas A&M Health Sciences Center College of Medicine, Temple, Texas 76502, USA.
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MeSH Terms
Acid-Base Equilibrium
Acidosis, Renal Tubular / etiology,  metabolism*
Aldosterone / blood
Angiotensin II / blood
Angiotensin Receptor Antagonists
Endothelins / blood
Glomerular Filtration Rate
Kidney Tubules, Distal / metabolism*
Mineralocorticoid Receptor Antagonists
Rats, Wistar
Receptor, Angiotensin, Type 2 / metabolism*
Receptors, Endothelin / antagonists & inhibitors,  metabolism
Receptors, Mineralocorticoid / metabolism
Renal Insufficiency / complications,  metabolism*
Reg. No./Substance:
0/Angiotensin Receptor Antagonists; 0/Endothelins; 0/Mineralocorticoid Receptor Antagonists; 0/Protons; 0/Receptor, Angiotensin, Type 2; 0/Receptors, Endothelin; 0/Receptors, Mineralocorticoid; 11128-99-7/Angiotensin II; 52-39-1/Aldosterone
Comment In:
Kidney Int. 2013 Jun;83(6):1204   [PMID:  23728010 ]
Kidney Int. 2013 Jun;83(6):1203-4   [PMID:  23728008 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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