HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 285/1/R255    most recent 00517.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Kong, J. Articles by Li, Y. C. Search for Related Content PubMed PubMed Citation Articles by Kong, J. Articles by Li, Y. C.

REGULATION IN GENETICALLY MODIFIED ANIMALS

Effect of ANG II type I receptor antagonist and ACE inhibitor on vitamin D receptor-null mice

Department of Medicine, University of Chicago, Chicago, Illinois 60637

Submitted 27 August 2002 ; accepted in final form 10 March 2003

We recently showed that vitamin D receptor (VDR) inactivation results in deregulated stimulation of the renin-angiotensin system (RAS). To address further the relation between RAS activation and the abnormalities in electrolyte and volume homeostasis, we studied the effect of the ANG II type I receptor antagonist losartan and the 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 wild-type and VDR-null mice, but renin expression remained much higher in the treated VDR-null mice than in the treated wild-type mice, suggesting that the ANG II feedback mechanism remains intact in the mutant mice. These data firmly established a causative relation between RAS overstimulation 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.

renin; captopril; losartan

This article has been cited by other articles:

				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]

				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]

				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]

				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]