Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 604, Issue 1-3, Pages 87-92Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2008.12.006
Keywords
Angiotensin II; Lipid accumulation; Lipotoxicity; Gene expression
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Funding
- Ministry of Education, Science, and Culture of Japan [19590937]
- Takeda Science Foundation, the Sankyo Foundation of Life Science
- Okinaka Memorial Institute for Medical Research
- Daiwa Securities Health Foundation
- Grants-in-Aid for Scientific Research [19590937] Funding Source: KAKEN
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Accumulation of lipids in the heart may cause cardiac dysfunction in various disorders, such as obesity and diabetes. In the current study, we have investigated whether administration of angiotensin II or norepinephrine induces accumulation of lipids and/or changes in the expression of genes related to lipid metabolism in the rat heart. Lipid deposition was found in myocardial, vascular wall, and perivascular cells of the angiotensin II-infused rat heart, and superoxide generation was increased in these lipid-positive cells. By contrast, intracardiac lipid deposition was not found in the heart of norepinephrine-induced hypertensive rats. Triglyceride content in the heart tissue of angiotensin II-infused rats increased more than 3-fold as compared with untreated controls. Losartan completely, but hydralazine only partially, suppressed the angiotensin II-induced intracardiac lipid deposition and increase in tissue triglyceride content. Administration of angiotensin II upregulated the mRNA expression of sterol regulatory element-binding protein-1c and fatty acid synthase, but downregulated that of uncoupling protein 2 and 3, in a manner dependent on the angiotensin AT, receptor. Collectively, these results suggest that angiotensin H may be involved in modulating both intracardiac lipid content and lipid metabolism-related gene expression, in part via an angiotensin AT, receptor-dependent and pressor-independent mechanism. (C) 2009 Elsevier B.V. All rights reserved.
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