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


     


Am J Physiol Renal Physiol 252: F221-F225, 1987;
0363-6127/87 $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 Cheema-Dhadli, S.
Right arrow Articles by Halperin, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cheema-Dhadli, S.
Right arrow Articles by Halperin, M. L.

AJP - Renal Physiology, Vol 252, Issue 2 221-F225, Copyright © 1987 by American Physiological Society


ARTICLES

Regulation of urea synthesis by acid-base balance in vivo: role of NH3 concentration

S. Cheema-Dhadli, R. L. Jungas and M. L. Halperin

The purpose of this study was to clarify how changes in acid-base balance influence the rate of urea synthesis in vivo. Since ureagenesis was increased by an ammonium infusion into rats, regulation seemed to be a function of the blood ammonium concentration. The rate of urea synthesis was constant at a fixed rate of ammonium infusion and independent of the conjugate base infused, chloride or bicarbonate. The steady-state blood ammonium concentration was higher in the rats that developed metabolic acidosis. Thus it appeared that regulation was not directly mediated by this ammonium concentration per se. The rate of urea synthesis was also independent of the blood pH. Accordingly, the rate of urea synthesis was examined as a function of the plasma NH3 concentration. The rate of ureagenesis was found to be directly proportional to the plasma NH3 concentration. Assuming that plasma NH3 levels reflect those in mitochondria, the NH3 concentration yielding half-maximal rates of urea synthesis (close to 2 microM) was in the same range as Km for the rate-limiting step in ureagenesis, carbamoyl phosphate synthetase (EC 6.3.4.16). These results suggest that, at a constant ammonium concentration, the decreased rate of ureagenesis caused by a pH fall in vitro could reflect an acidosis-induced decline in the concentration of true substrate (NH3) for this pathway.


This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
M. Hosch, J. Muser, H. N. Hulter, and R. Krapf
Ureagenesis: evidence for a lack of hepatic regulation of acid-base equilibrium in humans
Am J Physiol Renal Physiol, January 1, 2004; 286(1): F94 - F99.
[Abstract] [Full Text] [PDF]


Home page
Postgrad. Med. J.Home page
N. Thobe, P. Pilger, and M. P Jones
Primary hypothyroidism masquerading as hepatic encephalopathy: case report and review of the literature
Postgrad. Med. J., July 1, 2000; 76(897): 424 - 426.
[Abstract] [Full Text]




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