The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems
Abstract
Our recent studies suggest that 1,25-dihydroxyvitamin D 3 functions as an endocrine suppressor of renin biosynthesis. Genetic disruption of the vitamin D receptor (VDR) results in overstimulation of the renin-angiotensin system (RAS), leading to high blood pressure and cardiac hypertrophy. Consistent with the higher heart-to-body weight ratio, the size of left ventricular cardiomyocytes in VDR knockout (KO) mice was markedly increased compared with wild-type (WT) mice. As expected, levels of atrial natriuretic peptide (ANP) mRNA and circulating ANP were also increased in VDRKO mice. Treatment of VDRKO mice with captopril reduced cardiac hypertrophy and normalized ANP expression. To investigate the role of the cardiac RAS in the development of cardiac hypertrophy, the expression of renin, angiotensinogen, and AT-1a receptor in the heart was examined by real-time RT-PCR and immunostaining. In VDRKO mice, the cardiac renin mRNA level was significantly increased, and this increase was further amplified by captopril treatment. Consistently, intense immunostaining was detected in the left ventricle of captopril-treated WT and VDRKO mice by use of an anti-renin antibody. Levels of cardiac angiotensinogen and AT-1a receptor mRNAs were unchanged in the mutant mice. These data suggest that the cardiac hypertrophy seen in VDRKO mice is a consequence of activation of both the systemic and cardiac RAS and support the notion that 1,25-dihydroxyvitamin D 3 regulates cardiac functions, at least in part, through the RAS.
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Cites
1,25-Dihydroxyvitamin D3 is a negative endocrine regulator of the renin-angiotensin system
Li, Y. C., Kong, J., Wei, M., Chen, Z.-F., Liu, S. Q., & Cao, L.-P. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0215219 · Cited by 1,625
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Sunlight and Vitamin D: A global perspective for health
Wacker, M., & Holick, M. F. (2013) · Dermato-Endocrinology · doi:10.4161/derm.24494 · Cited by 1,156
Molecular Mechanisms of Vitamin D Action
Haussler, M. R., Whitfield, G. K., Kaneko, I., Haussler, C. A., Hsieh, D., Hsieh, J.-C., & Jurutka, P. W. (2013) · Calcified Tissue International · doi:10.1007/s00223-012-9619-0 · Cited by 759
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Witte, K. K., Byrom, R., Gierula, J., Paton, M. F., Jamil, H. A., Lowry, J. E., Gillott, R. G., Barnes, S. A., Chumun, H., Kearney, L. C., et al. (2016) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2016.03.508 · Cited by 229
Pathophysiology of calcium, phosphorus, and magnesium dysregulation in chronic kidney disease
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Calcitriol blunts the deleterious impact of advanced glycation end products on endothelial cells
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Deo, R., Katz, R., Shlipak, M. G., Sotoodehnia, N., Psaty, B. M., Sarnak, M. J., Fried, L. F., Chonchol, M., de Boer, I. H., Enquobahrie, D., et al. (2011) · Hypertension · doi:10.1161/hypertensionaha.111.179135 · Cited by 107
Michos, E. D., Streeten, E. A., Ryan, K. A., Rampersaud, E., Peyser, P. A., Bielak, L. F., Shuldiner, A. R., Mitchell, B. D., & Post, W. (2009) · Calcified Tissue International · doi:10.1007/s00223-008-9209-3 · Cited by 77
Calcium and Vitamin D Supplementation. Myths and Realities with Regard to Cardiovascular Risk
Muscogiuri, G., Barrea, L., Altieri, B., Di Somma, C., Bhattoa, H. P., Laudisio, D., Duval, G. T., Pugliese, G., Annweiler, C., Orio, F., et al. (2019) · Current Vascular Pharmacology · doi:10.2174/1570161117666190408165805 · Cited by 27
Metadata
- Authors
- Xiang, W., Kong, J., Chen, S., Cao, L.-P., Qiao, G., Zheng, W., Liu, W., Li, X., Gardner, D. G., & Li, Y. C.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2005-01
- Volume
- 288
- Issue
- 1
- Pages
- E125-E132
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2107865114
- Cited by
- 570
- References
- 1
- FWCI
- 7.23
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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