垂直傾斜時のプラズマエンドセリン: 矯正性低血圧に対する関連性?
H Kaufmann1, E Oribe, J A Oliver
1Department of Neurology, Mount Sinai School of Medicine, New York 10029.
Lancet (London, England)
|December 21, 1991
まとめ
バロレセプター反射の活性化は,おそらく神経低血圧から,プラズマにエンドセリンの放出を刺激する. エンドセリンの放出障害は,原発的自律不全における正静性低血圧に寄与する可能性があります.
科学分野:
- 心血管生理学 心血管の生理学
- エンドクリノロジー エンドクリノロジー
- 神経科学は神経科学である.
背景:
- 血のエンドセリン濃度は,直立した姿勢で上昇し,体積の膨張で減少します.
- バロレセプター反射は,血圧と液体のバランスを調節する上で重要な役割を果たします.
研究 の 目的:
- バロレセプター反射の活性化が,プラズマにエンドセリンの放出を誘発するかどうかを調査する.
- 姿勢の変化におけるバロレセプター機能とエンドセリン/バソプレシンレベルとの関係を調べる.
主な方法:
- プラズマのエンドセリンとバソプレシン濃度を,受動的垂直傾きで評価した.
- 4つのグループを研究した:正常な被験者,自律機能不全の患者,静脈血管性昏睡の患者,糖尿病不発症の患者.
主要な成果:
- 正常な被験者は,直立の傾きでエンドセリンとバソプレシンが増加した.
- 自律機能不全の患者は,血圧の低下にもかかわらず,エンドセリンの上昇はなかった.
- ヴァソヴァガル・シンコープの患者はエンドセリンとバソプレシンが増加し,糖尿病インシピドゥス患者はエンドセリン変化を示さなかった.
結論:
- バロレセプター反射の活性化は,潜在的にニューロヒポフィシスからのエンドセリン放出を誘発するようです.
- 欠陥のあるエンドセリンの放出は,原発的自律性障害で見られる正静性低血圧の要因である可能性があります.
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