Possible Linkage between Renal Injury and Cardiac Remodeling in Dahl Salt-Sensitive Rats Treated with the Calcium Channel Antagonist Benidipine.
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- Uehara Yoshio
- 2nd Department of Medicine, the University of Tokyo
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- Hirawa Nobuhito
- Department of Nephrology, Kantou-Teishin Hospital
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- Takeda Tsuyoshi
- Toxicological Research Laboratories, Kyowa Hakko Kogyo Co., Ltd.
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- Numabe Atsushi
- Department of Medicine, Dokkyo University School of Medicine
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- Kawabata Yukari
- 2nd Department of Medicine, the University of Tokyo
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- Nagoshi Hiroshi
- 2nd Department of Medicine, the University of Tokyo
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- Gomi Tomoko
- Department of Nephrology, Kantou-Teishin Hospital
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- Ikegami Jiro
- Toxicological Research Laboratories, Kyowa Hakko Kogyo Co., Ltd.
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- Goto Atsuo
- 2nd Department of Medicine, the University of Tokyo
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- Omata Masao
- 2nd Department of Medicine, the University of Tokyo
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Interest in cardiovascular protection by calcium channel antagonists has grown over the past decade. We investigated the prevention of cardiac remodeling and renal injury by the long-acting calcium channel antagonist benidipine using 12 week-old Dahl salt-sensitive (Dahl S) rats fed a high-salt (4% NaCl) diet. Six-week benidipine treatment (10mg/kg chow) decreased systolic blood pressure by 22% in Dahl S rats. This blood pressure reduction was associated with decreases in cardiac mass and weight of the aortic wall. Collagen content in the left ventricle tended to decline with benidipine treatment. In addition, glomerular filtration rate increased by 33% and arterial and glomerular lesions improved morphologically with this treatment. Regression of cardiac mass and collagen content in the left ventricle was due mainly to blood pressure reduction; however, collagen content in the low-pressure right ventricle was not only related to systemic blood pressure but to the severity of renal lesions. These data suggest that the calcium channel antagonist benidipine attenuates cardiac and renal injury in hypertensive Dahl S rats, and that part of the cardiac hypertrophy is due to a non-hemodynamic mechanism that might be responsible for, or be a consequence of, the lesions in the kidney. (Hypertens Res 1995; 18: 245-253)
収録刊行物
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- Hypertension Research
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Hypertension Research 18 (3), 245-253, 1995
日本高血圧学会
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詳細情報 詳細情報について
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- CRID
- 1390001204719135232
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- NII論文ID
- 130003456241
- 10010482464
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- NII書誌ID
- AA10847079
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- COI
- 1:CAS:528:DyaK28Xhsleguw%3D%3D
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- ISSN
- 13484214
- 09169636
- http://id.crossref.org/issn/09169636
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- PubMed
- 7584935
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 使用不可