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- Hayashi Koichi
- Department of Internal Medicine, School of Medicine, Keio University
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- Wakino Shu
- Department of Internal Medicine, School of Medicine, Keio University
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- Homma Koichiro
- Department of Internal Medicine, School of Medicine, Keio University
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- Sugano Naoki
- Department of Internal Medicine, School of Medicine, Keio University
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- Saruta Takao
- Department of Internal Medicine, School of Medicine, Keio University
書誌事項
- タイトル別名
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- Pathophysiological Significance of T-type Ca2+ Channels: Role of T-type Ca2+ Channels in Renal Microcirculation
- Role of T type Ca 2 Channels in Renal Microcirculation
この論文をさがす
抄録
Since conventional Ca2+ antagonists, with predominant blockade of L-type voltage-dependent Ca2+ channels, elicit preferential dilation of afferent arterioles, they might ostensibly aggravate glomerular hypertension. Recently, novel Ca2+ antagonists, with inhibitory action on L-/T-type Ca2+ channels, have been reported to dilate both afferent and efferent arterioles. The present review attempted to characterize the renal action of these Ca2+ antagonists and evaluated the consequences following the treatment with these agents. In contrast to conventional Ca2+ antagonists (e.g., nifedipine), novel antagonists (e.g., benidipine, efonidipine) potently dilated afferent and efferent arterioles; their action on efferent arterioles appeared to be mediated by the T-type Ca2+ channel blockade, probably through the inhibition of the intracellular Ca 2+ release. The comparison of the anti-proteinuric action in subtotally nephrectomized rats showed that efonidipine exerted more prominent action than nifedipine. Furthermore, Ca2+ antagonists with T-type Ca2+ inhibitory action inhibited renin/aldosterone release and proinflammatory process. Finally, patients with chronic renal disease given a 48-week efonidipine treatment showed reduced proteinuria, and this effect was seen even when mean arterial blood pressure failed to become less than 100 mmHg. Collectively, T-type Ca2+ channel blockade provides beneficial action in renal injury. Various mechanisms serve to protect against renal injury, including systemic/glomerular hemodynamic action and non-hemodynamic mechanisms.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 99 (3), 221-227, 2005
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
- 1390001205175420032
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- NII論文ID
- 10025731104
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- NII書誌ID
- AA11806667
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- COI
- 1:STN:280:DC%2BD2MnhsFentg%3D%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7709951
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- PubMed
- 16293936
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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