Special Feature

User Panel

My Panel

My Panel

Bookmark Science Articles

Recent News
Bookmark / Share This Science Site

Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice.

Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

  • Abstract Text of This Paper
  • Journal Published
  • MeSH Keywords of This Abstract
  • Chemicals and Substances Used in this Paper
  • Grants and Granting Agency of this Research
  • Database Accession Numbers Used in this Paper
  • Related Papers
  • Related Research Tags
  • Rate this Research Paper
  • Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Abstract Text:

    Hypertension is a major risk factor for cardiovascular disease. Thus, prevention of hypertension and consequent organ damage is important for reducing its incidence. In the present study, we examined the involvement of tissue inhibitor of metalloproteinase-3 (Timp-3) in N(omega)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension and accompanying vascular remodeling in mice. L-NAME was orally administered to wild-type (WT) and Timp-3 knockout (KO) mice for 6 weeks, blood pressure was monitored, and histological changes in myocardial arteries were examined. After L-NAME administration, blood pressure was lower in Timp-3 KO mice than in WT mice. The coronary arteries of WT and Timp-3 KO mice were similar after L-NAME treatment and showed no differences compared to untreated control mice. However, cardiac microvessels differed histologically between WT and Timp-3 KO mice. Vascular walls were less thickened in Timp-3 KO than in WT mice, and fibrotic changes were significantly reduced in Timp-3 KO mice. Moreover, the L-NAME-induced production of reactive oxygen species in cardiac microvessels was lower in Timp-3 KO than in WT mice. These results indicate that Timp-3 plays an important role in L-NAME-induced hypertension and myocardial vascular remodeling. Our findings suggest that Timp-3 may be a novel therapeutic target for the treatment of hypertension and consequent organ damage.

    Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Publishing Authors By Initials

    For similar proteins: tissue inhibitor of metalloproteinases: tissue inhibitor of metalloproteinase-3 research abstracts see: proteins: tissue inhibitor of metalloproteinases: tissue inhibitor of metalloproteinase-3 research

    PUBMED ID PMID:

    MEDLINE DATE:

    Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Journal Published:

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

    Journal: Hypertension research : official journal of the Ja

    VOLUME: 30

    Page Numbers: 563-71

    Journal Abbreviation: Hypertens. Res.

    ISSN: 0916-9636

    DAY: 3

    MONTH: Jun

    YEAR: 2007

    Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9307690

    Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Keywords Mesh Terms:

    KEYWORDS: Tissue Inhibitor of Metalloproteinase-3

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice. Information

    Substance Name: NG-Nitroarginine Methyl Ester

    Registry Number: 50903-99-6

    Grant and Affiliation Information for Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice.

    AFFILIATION: Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Suita, Japan.

    Country: Japan

    Japan Research PublicationJapan Research Publication

    AGENCY: United States NHLBI

    GRANT: HL42630

    ACRONYM: HL

    MEDLINETA: Hypertens Res

    REFSOURCE: Hypertens Res. 2007 Jun;30(6):477-8

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

    Tissue inhibitor of metalloproteinase-3 deficiency inhibits blood pressure elevation and myocardial microvascular remodeling induced by chronic administration of Nomega-nitro-L-arginine methyl ester in mice Related Publications

     

    Molecular Station USER Menu

    Welcome to Molecular Station!

    You have to register before you can post on our forums or use our advanced features. Register Now! Its Free and Fast!

    Already registered? Login now below.

    User Name:

    Password:

    Already registered and Forgot your password? Click below to recover it.

    Recover Lost Password

    Join now - it's fast and free!

    Molecular Station is THE largest network of researchers, scientists and science lovers anywhere!

    Research Terms of Usage and Disclaimer
    Home
    Features

    Protocols

    DNA Forum

    Science Forum

    DNA Forum
    Biology Forum

    Science News


    [CaRP] XML error: Invalid document end at line 2

    For more click here:Science News