| First Author | Kong J | Year | 2003 |
| Journal | Am J Physiol Regul Integr Comp Physiol | Volume | 285 |
| Issue | 1 | Pages | R255-61 |
| PubMed ID | 12637346 | Mgi Jnum | J:323298 |
| Mgi Id | MGI:7262809 | Doi | 10.1152/ajpregu.00517.2002 |
| Citation | Kong J, et al. (2003) Effect of ANG II type I receptor antagonist and ACE inhibitor on vitamin D receptor-null mice. Am J Physiol Regul Integr Comp Physiol 285(1):R255-61 |
| abstractText | 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. |
