Expression of endothelial nitric oxide synthase is suppressed in the renal vasculature of angiotensinogen-gene knockout mice |
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Authors: | Minoru Kihara Keiko Sato Tatsuo Hashimoto Nozomi Imai Yoshiyuki Toya Satoshi Umemura |
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Institution: | (1) Department of Internal Medicine II, School of Medicine, Yokohama City University, Kanazawa-ku, Yokohama 236-0004, Japan |
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Abstract: | We have attempted to elucidate the mechanism by which endothelial-type nitric oxide synthase (eNOS) is regulated in the kidney,
with special reference to the role of renal hemodynamics and angiotensin II (Ang II). We compared angiotensinogen gene knockout
(Atg−/−) mice, which lacked Ang II (resulting in sodium/water depletion and severe hypotension), with wild-type (Atg+/+) mice.
Using Western blot analysis and the NADPH diaphorase histochemical reaction, we found that the expression and activity of
eNOS were markedly lower in the renal vessels of Atg−/− mice compared with wild-type (Atg+/+) mice. Dietary salt loading significantly
enhanced renal eNOS levels and increased blood pressure in Atg−/− mice, but severe hypotension almost abolished the effects
of salt loading. In contrast, in Atg+/+ mice, altered salt intake or hydralazine had no effect on renal eNOS levels. These
results suggest that perfusion pressure plays an essential role in maintaining renal vascular eNOS activity, whereas Ang II
plays a supportive role, especially when renal circulation is impaired.
This study was supported by Grants-in-Aid for Scientific Resarch 2001–2003, Japan Society for Promotion of Science (grant
no. 13670735). |
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Keywords: | Kidney Nitric oxide synthase Angiotensin II Hypotension Dietary salt loading Perfusion pressure Mouse (ICR Atg+/+ Atg− /− ) |
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