Journal of the American Society of Nephrology
2007 JASN IMPACT FACTOR 7.111 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kleinman, J. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kleinman, J. G.

Journal of the American Society of Nephrology, Vol 5, S6-11, Copyright © 1994 by American Society of Nephrology

REVIEWS

Proton ATPases and urinary acidification

JG Kleinman
Medical College of Wisconsin, Section of Nephrology, Milwaukee.

Acidification of the urine is mediated by vectorial H+ transport from cells at a number of sites in the kidney. A proton ATPase has been described that appears to mediate a significant proportion of this H+ transport. In particular, in proximal tubule and collecting duct, there is evidence both for the presence of transporter protein and for H+ transport with features that have been identified with it. This review highlights some of the unresolved questions regarding this transporter, specifically, its distribution and relationship to the vacuolar pump present in endocytotic vesicles, how physiologic control is asserted, and its role in pathophysiology. The review discusses in greater detail the issue of whether the vacuolar H+ ATPase is responsible for all of the urinary acidification and concludes that it probably is not. Specifically, compelling evidence for acidification at sites in the kidney that appear to lack this transporter is presented. In addition, the evidence for the presence in the kidney of a gastric-type H(+)-K+ ATPase is also reviewed. The evidence appears to be strong for a K(+)- stimulated ATPase that is sensitive to omeprazole and SCH 28080, the prototypical H(+)-K+ ATPase inhibitors; however, uncertainties remain because of problems of transport inhibition specificity and discordant results of molecular biologic studies.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
T. Shibata, H. Hibino, K. Doi, T. Suzuki, Y. Hisa, and Y. Kurachi
Gastric type H+,K+-ATPase in the cochlear lateral wall is critically involved in formation of the endocochlear potential
Am J Physiol Cell Physiol, November 1, 2006; 291(5): C1038 - C1048.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
J. Suk Han, G.-H. Kim, J. Kim, U. Sil Jeon, K. Wook Joo, K. Young Na, C. Ahn, S. Kim, S. Eun Lee, and J. Sang Lee
Secretory-Defect Distal Renal Tubular Acidosis Is Associated with Transporter Defect in H+-ATPase and Anion Exchanger-1
J. Am. Soc. Nephrol., June 1, 2002; 13(6): 1425 - 1432.
[Abstract] [Full Text] [PDF]


HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673