Effect of exogenous nitric oxide on flow-induced endothelium-derived nitric oxide production

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  • Mochizuki Seiichi
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions
  • Sipkema Pieter
    Laboratory for Physiology, Vrije Universiteit Medical Center, Institute for Cardiovascular Research, Vrije Universiteit
  • Goto Masami
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions
  • Hiramatsu Osamu
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions
  • Nakamoto Hiroshi
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions
  • Toyota Eiji
    Department of Medical Engineering, Kawasaki Medical School
  • Yada Toyotaka
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions
  • Ogasawara Yasuo
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions
  • Kajiya Fumihiko
    Department of Medical Engineering, Kawasaki Medical School Department of Medical Engineering, Kawasaki College of Allied Health Professions

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Other Title
  • 外因性-酸化窒素(NO)による内皮細胞内テトラヒドロビオプテリンの減少を原因とする流れ依存性血管内皮由来NO産生の抑制
  • 外因性一酸化窒素(NO)による内皮細胞内テトラヒドロビオプテリンの減少を原因とする流れ依存性血管内皮由来NO産生の抑制
  • ガイインセイ 1サンカ チッソ NO ニ ヨル ナイヒ サイボウ ナイ テトラヒドロビオプテリン ノ ゲンショウ オ ゲンイン ト スル ナガレ イゾンセイ ケッカン ナイヒ ユライ NO サンセイ ノ ヨクセイ

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Abstract

We investigated the effect of exogenous nitric oxide (NO) on the flow-induced endothelium-derived NO production and possible underlying mechanisms including changes in intracellular concentration of tetrahydrobiopterin (BH4; a cofactor of NO synthase: NOS). Isolated canine femoral arteries were perfused with 100 μM S-nitroso-N-acetylpenicillamine (SNAP; an NO donor) and/or 64 μM BH4. Perfusion of SNAP suppressed flow-induced NO production (p<0.02 vs control; n=7). Subsequent BH4 perfusion restored the control-level NO production. Concomitant perfusion of SNAP and BH4 retained the control-level NO production. Concomitant perfusion of SNAP and 4,5- dihydroxy-1,3-benzene disulfonic acid (Tiron; 1 mM; a membrane-permeable superoxide scavenger) also retained the control-level NO production, while perfusion of Tiron after SNAP could not restore the control-level NO production (p<0.02 vs control; n=7). We also found a significant decrease in BH4 concentration in the endothelial cells after SNAP perfusion. In conclusion, these results indicate that exogenous NO decreases intracellular BH4 concentration, resulting in superox-ide release from uncoupled NOS and suppresses the flow-induced endothelium-derived NO produc-tion.

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