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Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases.

Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Research Abstract Details 

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  • Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Abstract Text:

    guo-xing zhangGuo-Xing Zhang,yukiko nagaiYukiko Nagai,toshitaka nakagawaToshitaka Nakagawa,hiroshi miyanakaHiroshi Miyanaka,yoshihide fujisawaYoshihide Fujisawa,akira nishiyamaAkira Nishiyama,kunihiko izuishiKunihiko Izuishi,koji ohmoriKoji Ohmori,shoji kimuraShoji Kimura,guo-xing zhangGuo-Xing Zhang,yukiko nagaiYukiko Nagai,toshitaka nakagawaToshitaka Nakagawa,hiroshi miyanakaHiroshi Miyanaka,yoshihide fujisawaYoshihide Fujisawa,akira nishiyamaAkira Nishiyama,kunihiko izuishiKunihiko Izuishi,koji ohmoriKoji Ohmori,shoji kimuraShoji Kimura,

    Angiotensin II (ANG II) is a powerful activator of mitogen-activated protein (MAP) kinase cascades in cardiovascular tissues through a redox-sensitive mechanism. Nitric oxide (NO) is considered to antagonize the vasoconstrictive and proarteriosclerotic actions of ANG II. However, the role of endogenous NO in ANG II-induced redox-sensitive signal transduction is not yet clear. In this study using catheterized, conscious rats, we found that acute intravenous administration of N(G)-nitro-L-arginine methyl ester (L-NAME; 5 mg/kg) enhanced phosphorylation of aortic MAP kinases extracellular signal regulated kinase (ERK) 1/2 and p38, which were suppressed only partially by a superoxide dismutase mimetic (Tempol), whereas ANG II-induced MAP kinase phosphorylation was markedly suppressed by Tempol. FK409, a NO donor, had little effect on vascular MAP kinase phosphorylation. On the other hand, acute exposure to a vasoconstrictor dose of ANG II (200 ng x kg(-1) x min(-1) iv) failed to enhance phosphorylation of aortic MAP kinases in the chronically L-NAME-treated rats, whereas the vasoconstrictor effect of ANG II was not affected by L-NAME treatment. Furthermore, three different inhibitors of NO synthase suppressed, in a dose-dependent manner, ANG II-induced MAP kinase phosphorylation in rat vascular smooth muscle cells, which was closely linked to superoxide generation in cells. These results indicate the involvement of endogenous NO synthase in ANG II-induced signaling pathways, leading to activation of MAP kinase, and that NO may have dual effects on the vascular MAP kinase activation associated with redox sensitivity.

    Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Publishing Authors By Initials

    gx zhangGX Zhang,y nagaiY Nagai,t nakagawaT Nakagawa,h miyanakaH Miyanaka,y fujisawaY Fujisawa,a nishiyamaA Nishiyama,k izuishiK Izuishi,k ohmoriK Ohmori,s kimuraS Kimura,gx zhangGX Zhang,y nagaiY Nagai,t nakagawaT Nakagawa,h miyanakaH Miyanaka,y fujisawaY Fujisawa,a nishiyamaA Nishiyama,k izuishiK Izuishi,k ohmoriK Ohmori,s kimuraS Kimura,

    For similar enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research abstracts see: enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research

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    Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Heart and circulat

    VOLUME: 293

    Page Numbers: H2403-8

    Journal Abbreviation: Am. J. Physiol. Heart Circ. Ph

    ISSN: 0363-6135

    DAY: 6

    MONTH: 07

    YEAR: 2007

    Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901228

    Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Keywords Mesh Terms:

    KEYWORDS: p38 Mitogen-Activated Protein Kinases

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases. Information

    Substance Name: p38 Mitogen-Activated Protein Kinases

    Registry Number: EC 2.7.1.37

    Grant and Affiliation Information for Involvement of endogenous nitric oxide in angiotensin II-induced activation of vascular mitogen-activated protein kinases.

    AFFILIATION: Department of Pharmacology, Kagawa University Medical School, Kagawa, Japan.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Am J Physiol Heart Circ Physio

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