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Am J Physiol Regul Integr Comp Physiol (March 13, 2003). doi:10.1152/ajpregu.00517.2002
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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.




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