心不全では細胞内ナトリウム濃度が上昇するが,Na/Kポンプの機能は変化しない
Sanda Despa1, Mohammed A Islam, Christopher R Weber
1Department of Physiology, Loyola University Chicago, Maywood, IL 60153, USA.
Circulation
|May 30, 2002
まとめ
心不全 (HF) の細胞内ナトリウム値上昇は,ナトリウム流入の増加によるもので,ナトリウム・カリウムポンプの機能障害によるものではない. このナトリウム増加は細胞カルシウム調節に影響を与え,HF患者における収縮機能障害を制限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
- 細胞電気生理学 細胞電気生理学
- 心不全 病理生理学 心不全 病理生理学
背景:
- 細胞内ナトリウム濃度 ([Na(+) ](i)) は,Na/Ca交換 (NCX) 機構を通じた心臓機能の重要な調節因子である.
- 心不全 (HF) の場合,NCXのアップレギュレーションは,心臓の収縮性および電気活動に対する変化した[Na+]の効果を拡大する可能性があります.
研究 の 目的:
- 心不全における細胞内ナトリウム濃度の上昇に起因するメカニズムを調査する.
- HFミオサイトにおける[Na(+) ](i) の調節におけるナトリウム流入と流出経路の役割を決定する.
主な方法:
- コントロールおよびHFモデルからウサギの心室筋細胞で,ナトリウム結合ベンゾフランイソフタラートを使用して,細胞内ナトリウム濃度 ([Na(+) ](i)) の測定.
- ポンプ機能を評価するために,Na/Kポンプ媒介のナトリウム挤出速度 (VmaxとKm) の評価.
- テトロドトキシンに敏感な経路を通る静止ナトリウム流入の定量化.
主要な成果:
- 休息中の細胞内ナトリウム濃度は,対照ミオサイト (6.6±0.5 mmol/L) と比較して,HFミオサイト (9.7±0.7 mmol/L) で有意に高かった.
- Na/Kポンプ機能 (VmaxとKm) はHFでは変化せず,通常のナトリウム挤出能力を示した.
- 休息中のナトリウム流入は,主にテトロドトキシンに敏感な経路経由で,HFミオサイトで倍増し,上昇した[Na(+) ](i) を説明しました.
結論:
- HFにおける細胞内ナトリウムの上昇は,正常なNa/K-ATPase活性で,ダイアストリックナトリウム流入の増加によるものです.
- HFの[Na(+) ](i) の増加は,変化したカルシウムトランジエントとアクションポテンシャルとともに,細胞のカルシウム処理とNCX活性に影響を与えます.
- 細胞内ナトリウム濃度の上昇は,心不全における重度の収縮機能不全を緩和することにより,保護的役割を果たす可能性があります.
キーワード:
非プログラム的なものです.関連する概念動画
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