AJP - Regu Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol (March 13, 2003). doi:10.1152/ajpregu.00517.2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
285/1/R255    most recent
00517.2002v1
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 Kong, J.
Right arrow Articles by Li, Y. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kong, J.
Right arrow Articles by Li, Y. C.
Submitted on August 27, 2002
Accepted on March 10, 2003

Effect of Angiotensin II Type I Receptor Antagonist and Angiotensin-Converting Enzyme Inhibitor on Vitamin D Receptor Null Mice

Juan Kong1 and Yan Chun Li1*

1 Department of Medicine, University of Chicago, Chicago, IL, USA

* To whom correspondence should be addressed. E-mail: cyan{at}medicine.bsd.uchicago.edu.

We have recently shown that vitamin D receptor (VDR) inactivation results in deregulated stimulation of the renin-angiotensin system (RAS). To address further the relationship between RAS activation and the abnormalities in electrolyte and volume homeostasis, we studied the effect of AT1 receptor antagonist losartan and angiotensin-converting enzyme inhibitor captopril on VDR-null mice. Treatment with losartan or captopril normalized the water intake and urine excretion of VDR-null mice. However, the increase in salt excretion in VDR-null mice was not affected by either drug, suggesting that this abnormality is independent of the RAS. Northern blot and immunohistochemical analyses revealed that both drugs caused a drastic stimulation of renin expression in both wild-type and VDR-null mice, but renin expression in the treated VDR-null mice remained much higher than in the treated wild-type mice, suggesting that the angiotensin (Ang)II feedback mechanism remains intact in the mutant mice. These data firmly established a causative relationship between RAS over-stimulation and the abnormal volume homeostasis in VDR-null mice, and demonstrated that vitamin D repression of renin expression is independent of the Ang II feedback regulation in vivo.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
Y. Zhang, D. K. Deb, J. Kong, G. Ning, Y. Wang, G. Li, Y. Chen, Z. Zhang, S. Strugnell, Y. Sabbagh, et al.
Long-term therapeutic effect of vitamin D analog doxercalciferol on diabetic nephropathy: strong synergism with AT1 receptor antagonist
Am J Physiol Renal Physiol, September 1, 2009; 297(3): F791 - F801.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
J. Kong, Z. Zhang, D. Li, K. E. Wong, Y. Zhang, F. L. Szeto, M. W. Musch, and Y. C. Li
Loss of Vitamin D Receptor Produces Polyuria by Increasing Thirst
J. Am. Soc. Nephrol., December 1, 2008; 19(12): 2396 - 2405.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
W. Yuan, W. Pan, J. Kong, W. Zheng, F. L. Szeto, K. E. Wong, R. Cohen, A. Klopot, Z. Zhang, and Y. C. Li
1,25-Dihydroxyvitamin D3 Suppresses Renin Gene Transcription by Blocking the Activity of the Cyclic AMP Response Element in the Renin Gene Promoter
J. Biol. Chem., October 12, 2007; 282(41): 29821 - 29830.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
W. Xiang, J. Kong, S. Chen, L.-P. Cao, G. Qiao, W. Zheng, W. Liu, X. Li, D. G. Gardner, and Y. C. Li
Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems
Am J Physiol Endocrinol Metab, January 1, 2005; 288(1): E125 - E132.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2003 by the American Physiological Society.