Pathophysiological Roles of Endothelin Receptors in Cardiovascular Diseases
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- Ohkita Mamoru
- Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, Japan
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- Tawa Masashi
- Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, Japan Department of Pharmacology, Shiga University of Medical Science, Japan
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- Kitada Kento
- Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, Japan Department of Pharmacology, Kagawa University Medical School, Japan
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- Matsumura Yasuo
- Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, Japan
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Endothelin (ET)-1 derived from endothelial cells has a much more important role in cardiovascular system regulation than the ET-2 and ET-3 isoforms. Numerous lines of evidence indicate that ET-1 possesses a number of biological activities leading to cardiovascular diseases (CVD) including hypertension and atherosclerosis. Physiological and pathophysiological responses to ET-1 in various tissues are mediated by interactions with ETA- and ETB-receptor subtypes. Both subtypes on vascular smooth muscle cells mediate vasoconstriction, whereas the ETB-receptor subtype on endothelial cells contributes to vasodilatation and ET-1 clearance. Although selective ETA- or nonselective ETA/ETB-receptor antagonisms have been assumed as potential strategies for the treatment of several CVD based on clinical and animal experiments, it remains unclear which antagonisms are suitable for individuals with CVD because upregulation of the nitric oxide system via the ETB receptor is responsible for vasoprotective effects such as vasodilatation and anti-cell proliferation. In this review, we have summarized the current understanding regarding the role of ET receptors, especially the ETB receptor, in CVD.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 119 (4), 302-313, 2012
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205180156160
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- NII論文ID
- 10031071269
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC38XhtlagtbrM
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 023892408
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- PubMed
- 22863667
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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
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可