ニューロンの酸化窒素合成酵素は,ヒトの基礎微血管トーンをin vivoで調節する
Michael D Seddon1, Philip J Chowienczyk, Sally E Brett
1Department of Cardiology, King's College London School of Medicine, 125 Coldharbour Ln, London SE5 9NU, United Kingdom.
Circulation
|April 9, 2008
まとめ
神経性酸化窒素合成酵素 (nNOS) は,ヒトの基礎前腕の血流を調節する. 内皮酸化窒素合成酵素 (eNOS) は主にアセチルコリン刺激による血管拡張を媒介し,血管調節における明確な役割を強調しています.
科学分野:
- 心血管生理学 心血管の生理学
- 血管生物学 血管生物学
- 酸化窒素シグナリング
背景:
- 酸化窒素 (NO) は,血管のトーンと血流の調節に不可欠です.
- 内皮 NO 合成酵素 (eNOS) は,血管内の NO の主要な源です.
- 新興の証拠は,神経 NO 合成酵素 (nNOS) も動脈に存在する可能性があることを示唆しています.
研究 の 目的:
- 人間における血管血流の局所的調節におけるnNOSの役割を調査する.
- 基礎血流と刺激血流に対するnNOSとeNOSの貢献を区別する.
主な方法:
- 健康な被験者に腕動脈注入を用いたヒトでの最初の研究です.
- nNOS特異的阻害剤 (SMTC) と非選択的NOS阻害剤 (L-NMMA) の投与.
- 基礎前腕の血流とアセチルコリンと精神的ストレスに対する反応の評価.
主要な成果:
- SMTCは,用量に依存して,前腕の基礎血流を最大30.1%まで減少させた.
- L-NMMAは,20倍の高用量で同様の減少を引き起こしました.
- SMTCは精神的なストレスに対する反応を抑制し,L-NMMAはアセチルコリン誘発の血管拡張を抑制した.
結論:
- 血管のnNOSは,基礎的な人間の前腕の血流を調節する上で明確な役割を果たします.
- eNOSは主にアセチルコリン刺激による血管拡張に起因する.
- nNOSは,微血管トーン調節に寄与する.
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