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- Katori Makoto
- Department of Pharmacology, Kitasato University School of Medicine, Japan
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- Majima Masataka
- Department of Pharmacology, Kitasato University School of Medicine, Japan
書誌事項
- タイトル別名
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- Missing Link Between a High Salt Intake and Blood Pressure Increase
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抄録
It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (KATP) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as KATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 100 (5), 370-390, 2006
公益社団法人 日本薬理学会
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詳細情報
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- CRID
- 1390282680153495680
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- NII論文ID
- 10018238332
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- NII書誌ID
- AA11806667
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- COI
- 1:STN:280:DC%2BD28zot1aluw%3D%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7963157
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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
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- 使用不可