Abnormal polyamine metabolism in hypertensive cardiac hypertrophy
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- SHIMIZU M.
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- MASUDA IZURU
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- AIHARA KAZUO
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- NAKANO TOMOKO
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- OGAWA KAZUHIKO
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- MIZOKAMI TSUNEO
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- IRIMAJIRI OSAMU
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- TANIGUCHI IKUO
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- OZASA HARUKI
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- KAGEYAMA SHIGERU
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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- HAYASHI SHIN-ICHI
- Department of Nutrition, The Jikei University School of Medicine
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- ISOGAI YUKIHIDE
- The Third Department of Internal Medicine, The Jikei University School of Medicine
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抄録
In order to assess myocardial hypertrophic activity during the process of hypertensive cardiac hypertrophy in the presence and absence of treatment with anti-hypertensive agents, we analyzed myocardial polyamine concentrations in spontaneous hypertensive (SHR) rats and control rats of Wistar Kyoto (WKY) strain. The anti-hypertensive agents studied were diltiazem, hydralazine and captopril, each of which was administered for 5 weeks. In comparison with WKY rats, SHR rats showed elevated blood pressure and enlarged hearts with higher myocardial spermidine concentration. Although blood pressure was lowered in the diltiazem-treated SHR rats, heart weight and myocardial spermidine concentration increased as in untreated SHR rats. In the hydralazine-treated group increases in both blood pressure and myocardial spermidine concentration were all suppressed. Since spermidine level appears to be a sensitive indicator of hypertrophic activity in the heart, this study suggests that captopril exerts an inhibitory effect on hypertensive cardiac hypertrophy whereas diltiazem does not. It also suggests that hypertrophy may reach a certain plateau level earlier in the hydralazine-treated animals than in others.
収録刊行物
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- Jpn Circ J
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Jpn Circ J 52 1209-1215, 1988
社団法人日本循環器学会
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詳細情報 詳細情報について
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- CRID
- 1572824501998291840
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- NII論文ID
- 110002630849
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- NII書誌ID
- AA00690731
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- ISSN
- 00471828
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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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- CiNii Articles