A Missing Link Between a High Salt Intake and Blood Pressure Increase

DOI Web Site PubMed 被引用文献1件 参考文献290件 オープンアクセス
  • Katori Makoto
    Department of Pharmacology, Kitasato University School of Medicine, Japan
  • Majima Masataka
    Department of Pharmacology, Kitasato University School of Medicine, Japan

書誌事項

タイトル別名
  • Missing Link Between a High Salt Intake and Blood Pressure Increase
公開日
2006
DOI
  • 10.1254/jphs.crj06003x
公開者
公益社団法人 日本薬理学会

この論文をさがす

説明

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

被引用文献 (1)*注記

もっと見る

参考文献 (290)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ