Increased prostanoid dependency of arterial relaxation in Chlamydia pneumoniae-infected mice

Liisa Törmäkangas, Juha Ketonen, Maija Leinonen, Pekka Saikku, Ilari Paakkari

    Research output: Contribution to journalArticleScientificpeer-review

    Abstract

    Endothelial dysfunction plays an important role in the development of atherosclerosis. Previous studies have shown that inoculation with Chlamydia pneumoniae contributes to atherosclerotic development in rabbits and hypercholesterolaemic mice and causes endothelial dysfunction in apolipoprotein E-deficient mice. The effect of acute C. pneumoniae infection on endothelial function in normocholesterolaemic C57BL/6J mice was studied by measuring the force of contraction of the descending aorta after noradrenaline stimulation and in response to methacholine-induced relaxation. In addition, the effects of the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) and the cyclooxygenase inhibitor diclofenac on relaxation were assessed. Pre-treatment of the aortas with L-NAME decreased the relaxation response in both the infected and uninfected groups and no significant difference was detected between these groups, whereas diclofenac significantly attenuated the relaxation response only in the infected animals. In conclusion, infection shifted the balance of endothelium-derived relaxing factors from nitric oxide towards vasorelaxing prostanoids in C57BL/6J mice.
    Original languageEnglish
    JournalJournal of Medical Microbiology
    Volume55
    Pages (from-to)1017-1021
    Number of pages5
    ISSN0022-2615
    DOIs
    Publication statusPublished - 2006
    MoE publication typeA1 Journal article-refereed

    Cite this

    @article{750ce44129214812977b9871e6a0c9e6,
    title = "Increased prostanoid dependency of arterial relaxation in Chlamydia pneumoniae-infected mice",
    abstract = "Endothelial dysfunction plays an important role in the development of atherosclerosis. Previous studies have shown that inoculation with Chlamydia pneumoniae contributes to atherosclerotic development in rabbits and hypercholesterolaemic mice and causes endothelial dysfunction in apolipoprotein E-deficient mice. The effect of acute C. pneumoniae infection on endothelial function in normocholesterolaemic C57BL/6J mice was studied by measuring the force of contraction of the descending aorta after noradrenaline stimulation and in response to methacholine-induced relaxation. In addition, the effects of the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) and the cyclooxygenase inhibitor diclofenac on relaxation were assessed. Pre-treatment of the aortas with L-NAME decreased the relaxation response in both the infected and uninfected groups and no significant difference was detected between these groups, whereas diclofenac significantly attenuated the relaxation response only in the infected animals. In conclusion, infection shifted the balance of endothelium-derived relaxing factors from nitric oxide towards vasorelaxing prostanoids in C57BL/6J mice.",
    author = "Liisa T{\"o}rm{\"a}kangas and Juha Ketonen and Maija Leinonen and Pekka Saikku and Ilari Paakkari",
    year = "2006",
    doi = "10.1099/jmm.0.46516-0",
    language = "English",
    volume = "55",
    pages = "1017--1021",
    journal = "Journal of Medical Microbiology",
    issn = "0022-2615",
    publisher = "SOCIETY FOR GENERAL MICROBIOLOGY",

    }

    Increased prostanoid dependency of arterial relaxation in Chlamydia pneumoniae-infected mice. / Törmäkangas, Liisa; Ketonen, Juha; Leinonen, Maija; Saikku, Pekka; Paakkari, Ilari.

    In: Journal of Medical Microbiology, Vol. 55, 2006, p. 1017-1021.

    Research output: Contribution to journalArticleScientificpeer-review

    TY - JOUR

    T1 - Increased prostanoid dependency of arterial relaxation in Chlamydia pneumoniae-infected mice

    AU - Törmäkangas, Liisa

    AU - Ketonen, Juha

    AU - Leinonen, Maija

    AU - Saikku, Pekka

    AU - Paakkari, Ilari

    PY - 2006

    Y1 - 2006

    N2 - Endothelial dysfunction plays an important role in the development of atherosclerosis. Previous studies have shown that inoculation with Chlamydia pneumoniae contributes to atherosclerotic development in rabbits and hypercholesterolaemic mice and causes endothelial dysfunction in apolipoprotein E-deficient mice. The effect of acute C. pneumoniae infection on endothelial function in normocholesterolaemic C57BL/6J mice was studied by measuring the force of contraction of the descending aorta after noradrenaline stimulation and in response to methacholine-induced relaxation. In addition, the effects of the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) and the cyclooxygenase inhibitor diclofenac on relaxation were assessed. Pre-treatment of the aortas with L-NAME decreased the relaxation response in both the infected and uninfected groups and no significant difference was detected between these groups, whereas diclofenac significantly attenuated the relaxation response only in the infected animals. In conclusion, infection shifted the balance of endothelium-derived relaxing factors from nitric oxide towards vasorelaxing prostanoids in C57BL/6J mice.

    AB - Endothelial dysfunction plays an important role in the development of atherosclerosis. Previous studies have shown that inoculation with Chlamydia pneumoniae contributes to atherosclerotic development in rabbits and hypercholesterolaemic mice and causes endothelial dysfunction in apolipoprotein E-deficient mice. The effect of acute C. pneumoniae infection on endothelial function in normocholesterolaemic C57BL/6J mice was studied by measuring the force of contraction of the descending aorta after noradrenaline stimulation and in response to methacholine-induced relaxation. In addition, the effects of the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) and the cyclooxygenase inhibitor diclofenac on relaxation were assessed. Pre-treatment of the aortas with L-NAME decreased the relaxation response in both the infected and uninfected groups and no significant difference was detected between these groups, whereas diclofenac significantly attenuated the relaxation response only in the infected animals. In conclusion, infection shifted the balance of endothelium-derived relaxing factors from nitric oxide towards vasorelaxing prostanoids in C57BL/6J mice.

    U2 - 10.1099/jmm.0.46516-0

    DO - 10.1099/jmm.0.46516-0

    M3 - Article

    VL - 55

    SP - 1017

    EP - 1021

    JO - Journal of Medical Microbiology

    JF - Journal of Medical Microbiology

    SN - 0022-2615

    ER -