AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 251: R859-R866, 1986;
0363-6119/86 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Welbourne, T. C.
Right arrow Articles by Givens, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Welbourne, T. C.
Right arrow Articles by Givens, G.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 5 859-R866, Copyright © 1986 by American Physiological Society


ARTICLES

Renal regulation of interorgan glutamine flow in metabolic acidosis

T. C. Welbourne, D. Childress and G. Givens

The regulation of interorgan glutamine flow was studied in control and chronically metabolically acidotic rats. Net glutamine extraction or production across the kidneys, gut, liver, and hindquarters was determined in fasted anesthetized animals from organ blood flows and the arteriovenous glutamine concentration difference. In control animals glutamine flows from the hindquarters to the splanchnic bed. In chronic acidosis glutamine production by the hindquarters rose threefold and was redirected to the kidneys; splanchnic bed glutamine uptake was eliminated. Associated with this was a 39% fall and a 62% rise in arterial glutamine and ammonia concentrations, respectively. Removing the kidneys from the circulation returned arterial glutamine and ammonia concentrations to control nonacidotic levels within 30 min. Net glutamine production by the hindquarters decreased, whereas splanchnic bed glutamine extraction increased. Hindquarter glutamine production appears to be modulated by renal venous ammonia; splanchnic bed glutamine extraction is load dependent, reflecting the influence of renal glutamine consumption on the steady-state arterial levels. Thus the removal of the kidneys returns interorgan glutamine flow to that observed in nonacidotic animals consistent with a major role of the kidneys in regulating glutamine flow and nitrogen metabolism in chronic metabolic acidosis.


This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
C. Moret, M. H. Dave, N. Schulz, J. X. Jiang, F. Verrey, and C. A. Wagner
Regulation of renal amino acid transporters during metabolic acidosis
Am J Physiol Renal Physiol, February 1, 2007; 292(2): F555 - F566.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online