The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Pressure Overload Induces Cardiac Hypertrophy in Angiotensin II Type 1A Receptor Knockout Mice
Open accessAbstract
Background—Many studies have suggested that the renin-angiotensin system plays an important role in the development of pressure overload–induced cardiac hypertrophy. Moreover, it has been reported that pressure overload–induced cardiac hypertrophy is completely prevented by ACE inhibitors in vivo and that the stored angiotensin II (Ang II) is released from cardiac myocytes in response to mechanical stretch and induces cardiomyocyte hypertrophy through the Ang II type 1 receptor (AT 1) in vitro. These results suggest that the AT 1-mediated signaling is critical for the development of mechanical stress–induced cardiac hypertrophy. Methods and Results—To determine whether AT 1-mediated signaling is indispensable for the development of pressure overload–induced cardiac hypertrophy, pressure overload was produced by constricting the abdominal aorta of AT 1A knockout (KO) mice. Quantitative reverse transcriptase–polymerase chain reaction revealed that the cardiac AT 1(probably AT 1B) mRNA levels in AT 1A KO mice were <10% of those of wild-type (WT) mice and were not affected by pressure overload. Chronic treatment with subpressor doses of Ang II increased left ventricular mass in WT mice but not in KO mice. Pressure overload, however, fully induced cardiac hypertrophy in KO as well as WT mice. There were no significant differences between WT and KO mice in expression levels of fetal-type cardiac genes, in the left ventricular wall thickness and systolic function as revealed by the transthoracic echocardiogram, or in the histological changes such as myocyte hypertrophy and fibrosis. Conclusions—AT 1-mediated Ang II signaling is not essential for the development of pressure overload–induced cardiac hypertrophy.
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Cites
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Cited by
Left Ventricular Hypertrophy: Pathogenesis, Detection, and Prognosis
Lorell, B. H., & Carabello, B. A. (2000) · Circulation · doi:10.1161/01.cir.102.4.470 · Cited by 1,232
TGF-β1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II
Schultz, J. E. J., Witt, S. A., Glascock, B. J., Nieman, M. L., Reiser, P. J., Nix, S. L., Kimball, T. R., & Doetschman, T. (2002) · Journal of Clinical Investigation · doi:10.1172/jci14190 · Cited by 426
Yamamoto, K., Ohishi, M., Katsuya, T., Ito, N., Ikushima, M., Kaibe, M., Tatara, Y., Shiota, A., Sugano, S., Takeda, S., et al. (2006) · Hypertension · doi:10.1161/01.hyp.0000205833.89478.5b · Cited by 323
Metadata
- Authors
- Harada, K., Komuro, I., Shiojima, I., Hayashi, D., Kudoh, S., Mizuno, T., Kijima, K., Matsubara, H., Sugaya, T., Murakami, K., & Yazaki, Y.
- Venue
- Circulation
- Published
- 1998-05-19
- Volume
- 97
- Issue
- 19
- Pages
- 1952-1959
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2004775541
- Cited by
- 254
- References
- 45
- FWCI
- 17.57
- Type
- journal article
- Language
- en
- Open access
- bronze
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- The paper
- Harada, K., Komuro, I., Shiojima, I., Hayashi, D., Kudoh, S., Mizuno, T., Kijima, K., Matsubara, H., Sugaya, T., Murakami, K., & Yazaki, Y. (1998). Pressure Overload Induces Cardiac Hypertrophy in Angiotensin II Type 1A Receptor Knockout Mice. Circulation. https://doi.org/10.1161/01.cir.97.19.1952
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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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