Fibrotic response to angiotensin II is blunted in the kidney, but not in the heart, in insulin-sensitive long-lived transgenic dwarf rats

Sato,Osami; Ashizawa,Naoto; Ohtsuru,Akira; Imanishi,Ryo; Kawano,Hiroaki; Seto,Shinji; Yamashita,Shunichi; Shimokawa,Isao; Yano,Katsusuke

doi:10.3892/ijmm.19.1.23

January 2007 Volume 19 Issue 1

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January 2007 Volume 19 Issue 1

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Article

Fibrotic response to angiotensin II is blunted in the kidney, but not in the heart, in insulin-sensitive long-lived transgenic dwarf rats

Authors:
- Osami Sato
- Naoto Ashizawa
- Akira Ohtsuru
- Ryo Imanishi
- Hiroaki Kawano
- Shinji Seto
- Shunichi Yamashita
- Isao Shimokawa
- Katsusuke Yano
View Affiliations / Copyright

Affiliations: Division of Cardiovascular Medicine, Course of Medical and Dental Sciences, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan
Pages: 23-27
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Published online on: January 1, 2007

https://doi.org/10.3892/ijmm.19.1.23
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Abstract

Insulin resistance is a characteristic feature of cardiovascular and renal diseases, and angiotensin II (Ang II) has been suggested to induce insulin resistance. The aims of this study were to elucidate the effect of chronic Ang II infusion on vascular reactivity and organ damage in insulin-sensitive rats. We confirmed the following three points. First, there was no significant difference in pressor response to chronic Ang II infusion (600 ng/kg/min) between insulin-sensitive transgenic rats (Tg) and control rats (C). Second, there was no significant difference in cardiac hypertrophy and fibrosis by chronic Ang II infusion between the two groups. However, third, fibrotic response to chronic Ang II infusion evaluated by histopathological scoring in the kidney was significantly decreased in insulin-sensitive transgenic rats (renal fibrosis and nephropathy score: C+Ang II vs Tg+Ang II; 2.5 vs 1.3; p<0.05). Furthermore, the expression of TGF-β, a fibrosis indicator, was also significantly suppressed in the kidneys of the transgenic rats (TGF-β1/GAPDH ratio: C+Ang II vs Tg+Ang II; 1.15 vs 0.81; p<0.05). This result indicates that the growth hormone/insulin-like growth factor-1 axis is critically involved in the development of renal injury and fibrosis, rather than hypertension, cardiac hypertrophy, and cardiac fibrosis induced by chronic Ang II administration.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Fibrotic response to angiotensin II is blunted in the kidney, but not in the heart, in insulin-sensitive long-lived transgenic dwarf rats

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