アンジオテンシンII. アドレネージ的交感性コンストリクター作用は,ヒトにおける
D Lyons1, J Webster, N Benjamin
1Clinical Age Research Unit, Kings College Hospital, Denmark Hill, London, UK.
Circulation
|March 1, 1995
まとめ
アンジオテンシンII (Ang II) は,人間における交感神経系の活性化による部分的な血管収縮を引き起こす. アルファ受容体をフェントオラミンでブロックすると,ニトロプロシドと比較して,前腕の血流に対するAng IIの効果が低下する.
科学分野:
- 心血管生理学 心血管の生理学
- 神経内分泌学の神経内分泌学
背景:
- アンジオテンシンII (Ang II) は,アドレナージ神経伝達に作用する.
- アンジオテンシン変換酵素阻害剤は,カテキオラミン濃度に影響を与える可能性があります.
- Ang IIの血管圧縮効果は,ヒトでのさらなる調査を必要としています.
研究 の 目的:
- Ang II誘発の血管収縮における交感的メディエーションの役割を調査する.
- アルファ受容体阻害時の前腕の血流に対するAng IIの効果と血管拡張の効果を比較する.
主な方法:
- 健康なボランティアの腕動脈にAng IIの局所性静脈内注入.
- フェントオラミンによるポストシナプスアルファ受容体の薬理学的阻害.
- ニトロプロシド誘発性血管拡張中のAng II輸液との比較.
- 前腕の血流の測定は,ストレインゲージ・プレチスモグラフィを用いて行います.
主要な成果:
- Ang IIによる前腕の血流の減少は,ニトロプロシド血管拡張 (52.9%) と比較して,フェントオラミン阻害 (28.1%) の間,著しく低下しました.
- 血流に対するAng IIの用量反応曲線の傾きは,ニトロプロシド投与時 (−0.16) よりも,フェントアミン阻害 (−0.098) 時に著しく鈍かった.
結論:
- 人間の前腕の抵抗性血管に対する外因的なAng IIの血管圧縮作用の大部分は,交感経路によって媒介されます.
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