骨格筋のカプサイシン感受性アフェレントニューロンは,心不全で異常である
Scott A Smith1, Maurice A Williams, Jere H Mitchell
1Department of Internal Medicine, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, TX 75390-9174, USA.
Circulation
|April 27, 2005
まとめ
心不全は,変化したグループIVアファレントニューロンにより,運動圧力反射 (EPR) を悪化させる. これらのニューロンは,膨張性心筋病変において鈍感な反応を示し,EPR機能不全と運動能力の低下に寄与します.
科学分野:
- 心血管生理学 心血管の生理学
- 神経科学は神経科学である.
- 運動生理学 運動生理学
背景:
- 運動圧力反射 (EPR) は,心不全で誇張されています.
- 筋肉の代謝産物によって刺激されるグループIVアフェレントニューロンは,EPRに重要な貢献者である.
- これらのニューロンの変異は,心不全におけるEPR機能不全の根底にある可能性があります.
研究 の 目的:
- 心不全で観察される誇張されたEPRにおけるグループIVアフェレントニューロンの役割を調査する.
- グループIVニューロンの機能的および分子的変化が心不全モデルにおけるEPR機能障害に寄与するかどうかを判断する.
主な方法:
- グループIVのアフェレント繊維は,キャプサイシンを用いて新生ラットで切除された.
- EPRは,成人ネズミの電気誘導による静的な筋肉収縮によって活性化されました.
- 静脈内カプサイシンとTRPv1 mRNA発現に対する圧力器の反応を評価した.
主要な成果:
- 新生児のカプサイシン治療は,拡張性心筋症候群 (DCM) のラットで観察された誇張された心拍数と血圧の反応を模倣しました.
- カプサイシンで治療されたラットとDCMラットの両方,後肢カプサイシン投与に対する圧力反応が低下した.
- グループIV繊維のマーカーであるTRPv1mRNA発現は,DCMラットでダウンレギュレーションされた.
結論:
- 心不全におけるEPR機能障害は,グループIVアフェレント繊維の機能的および分子的変化を含む.
- これらの代謝的に敏感なニューロンの反応性は,全体的なEPRの誇張にもかかわらず,DCMでは鈍化しています.
- これらのメカニズムを理解することは,心不全における運動能力を改善する治療法の開発に不可欠です.
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