Nitric oxide synthesis inhibitors attenuate calcitonin gene-related peptide endothelium-dependent vasorelaxation in rat aorta

David W. Gray, Ian Marshall

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    Abstract

    The effect of inhibitors of nitric oxide synthesis were examined on the endothelium-dependent relaxation induced by acetylcholine and human alpha-calcitonin gene-related peptide (CGRP) on rat isolated aortic rings preconstricted with noradrenaline. The endothelium-dependent vasorelaxation induced by acetylcholine and CGRP was inhibited by NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NOARG) in a concentration-related fashion. The inhibition of endothelium-dependent relaxation by L-NMMA and L-NOARG was partially reversed by L-arginine but not by D-arginine for both acetylcholine and CGRP. The data presented suggests that CGRP, like acetylcholine; relaxes the rat aorta via the release of nitric oxide.

    Original languageEnglish
    Pages (from-to)37-42
    Number of pages6
    JournalEuropean Journal of Pharmacology
    Volume212
    Issue number1
    DOIs
    Publication statusPublished - 1992

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    omega-N-Methylarginine
    Calcitonin Gene-Related Peptide
    Vasodilation
    Acetylcholine
    Endothelium
    Aorta
    Nitric Oxide
    Nitroarginine
    Arginine
    Norepinephrine

    Cite this

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    title = "Nitric oxide synthesis inhibitors attenuate calcitonin gene-related peptide endothelium-dependent vasorelaxation in rat aorta",
    abstract = "The effect of inhibitors of nitric oxide synthesis were examined on the endothelium-dependent relaxation induced by acetylcholine and human alpha-calcitonin gene-related peptide (CGRP) on rat isolated aortic rings preconstricted with noradrenaline. The endothelium-dependent vasorelaxation induced by acetylcholine and CGRP was inhibited by NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NOARG) in a concentration-related fashion. The inhibition of endothelium-dependent relaxation by L-NMMA and L-NOARG was partially reversed by L-arginine but not by D-arginine for both acetylcholine and CGRP. The data presented suggests that CGRP, like acetylcholine; relaxes the rat aorta via the release of nitric oxide.",
    author = "Gray, {David W.} and Ian Marshall",
    year = "1992",
    doi = "10.1016/0014-2999(92)90069-G",
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    journal = "European Journal of Pharmacology",
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    TY - JOUR

    T1 - Nitric oxide synthesis inhibitors attenuate calcitonin gene-related peptide endothelium-dependent vasorelaxation in rat aorta

    AU - Gray, David W.

    AU - Marshall, Ian

    PY - 1992

    Y1 - 1992

    N2 - The effect of inhibitors of nitric oxide synthesis were examined on the endothelium-dependent relaxation induced by acetylcholine and human alpha-calcitonin gene-related peptide (CGRP) on rat isolated aortic rings preconstricted with noradrenaline. The endothelium-dependent vasorelaxation induced by acetylcholine and CGRP was inhibited by NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NOARG) in a concentration-related fashion. The inhibition of endothelium-dependent relaxation by L-NMMA and L-NOARG was partially reversed by L-arginine but not by D-arginine for both acetylcholine and CGRP. The data presented suggests that CGRP, like acetylcholine; relaxes the rat aorta via the release of nitric oxide.

    AB - The effect of inhibitors of nitric oxide synthesis were examined on the endothelium-dependent relaxation induced by acetylcholine and human alpha-calcitonin gene-related peptide (CGRP) on rat isolated aortic rings preconstricted with noradrenaline. The endothelium-dependent vasorelaxation induced by acetylcholine and CGRP was inhibited by NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NOARG) in a concentration-related fashion. The inhibition of endothelium-dependent relaxation by L-NMMA and L-NOARG was partially reversed by L-arginine but not by D-arginine for both acetylcholine and CGRP. The data presented suggests that CGRP, like acetylcholine; relaxes the rat aorta via the release of nitric oxide.

    U2 - 10.1016/0014-2999(92)90069-G

    DO - 10.1016/0014-2999(92)90069-G

    M3 - Article

    C2 - 1555637

    VL - 212

    SP - 37

    EP - 42

    JO - European Journal of Pharmacology

    JF - European Journal of Pharmacology

    SN - 0014-2999

    IS - 1

    ER -