{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T05:42:17Z","timestamp":1785303737299,"version":"3.55.0"},"reference-count":28,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.1152\/ajpregu.00517.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:29:44Z","timestamp":1425414584000},"page":"R255-R261","source":"Crossref","is-referenced-by-count":69,"title":["Effect of ANG II type I receptor antagonist and ACE inhibitor on vitamin D receptor-null mice"],"prefix":"10.1152","volume":"285","author":[{"given":"Juan","family":"Kong","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Chicago, Chicago, Illinois 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan Chun","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Chicago, Chicago, Illinois 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"crossref","unstructured":"Agus ZS, Gardner LB, Beck LH, and Goldberg M.Effects of parathyroid hormone on renal tubular reabsorption of calcium, sodium, and phosphate.Am J Physiol224: 1143\u20131148, 1973.","DOI":"10.1152\/ajplegacy.1973.224.5.1143"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1007\/s001090000089"},{"key":"REF3","unstructured":"Ballermann BJ, Zeidel ML, Gunning ME, and Brenner BM.Vasoactive peptides and the kidney. 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