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


     

Am J Physiol Gastrointest Liver Physiol 269: G861-G866, 1995;
0193-1857/95 $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 Pastor, C. M.
Right arrow Articles by Billiar, T. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pastor, C. M.
Right arrow Articles by Billiar, T. R.

AJP - Gastrointestinal and Liver Physiology, Vol 269, Issue 6 861-G866, Copyright © 1995 by American Physiological Society

ARTICLES

Sources of arginine for induced nitric oxide synthesis in the isolated perfused liver

C. M. Pastor, S. M. Morris Jr and T. R. Billiar
Department of Surgery, University of Pittsburgh, Pennsylvania 15261, USA.

Hepatocytes can be stimulated to express high levels of inducible nitric oxide synthase (iNOS), which utilizes arginine for nitric oxide (NO) synthesis. Hepatocytes also synthesize and catabolize arginine, an intermediate in the urea cycle, raising the possibility that the urea pathway may provide substrate for hepatic NO synthesis. To identify the sources of arginine for iNOS, we measured the release of NO-2 + NO-3 and urea in isolated rat livers perfused in a recirculation model with a Krebs-Henseleit-bicarbonate buffer containing either no added amino acid, arginine, or precursors for urea synthesis. To induce iNOS expression, rats were injected with killed Corynebacterium parvum (C. parvum) or with endotoxin. In livers from C. parvum- and endotoxin-treated rats, we found that 1) an intracellular source of arginine exists that provides substrate to iNOS; 2) additional exogenous arginine increase NO synthesis, demonstrating that endogenous arginine is insufficient for maximal NO synthesis; and 3) an increase in the rate of endogenous arginine synthesis within the urea cycle is inefficient in increasing NO synthesis, demonstrating the independence of the two pathways in the liver.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. M. Reid, A. Tsung, T. Kaizu, G. Jeyabalan, A. Ikeda, L. Shao, G. Wu, N. Murase, and D. A. Geller
Liver I/R injury is improved by the arginase inhibitor, N{omega}-hydroxy-nor-L-arginine (nor-NOHA)
Am J Physiol Gastrointest Liver Physiol, February 1, 2007; 292(2): G512 - G517.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. M. Pastor, D. Williams, T. Yoneyama, K. Hatakeyama, S. Singleton, E. Naylor, and T. R. Billiar
Competition for Tetrahydrobiopterin between Phenylalanine Hydroxylase and Nitric Oxide Synthase in Rat Liver
J. Biol. Chem., October 4, 1996; 271(40): 24534 - 24538.
[Abstract] [Full Text] [PDF]


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