دورية أكاديمية
Chronic mild hyperhomocysteinemia induces aortic endothelial dysfunction but does not elevate arterial pressure in rats.
| العنوان: | Chronic mild hyperhomocysteinemia induces aortic endothelial dysfunction but does not elevate arterial pressure in rats. |
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| المؤلفون: | Miao CY; Cardiovascular Research Division, SERVIER Research Institute, FR-92150 Suresnes, France., Villeneuve N, Brunel-Jacquemin C, Petit C, Guillaumin JP, Gransagne D, Briant C, Vilaine JP, Vanhoutte PM |
| المصدر: | Journal of vascular research [J Vasc Res] 2005 Mar-Apr; Vol. 42 (2), pp. 148-56. Date of Electronic Publication: 2005 Feb 15. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: S. Karger Country of Publication: Switzerland NLM ID: 9206092 Publication Model: Print-Electronic Cited Medium: Print ISSN: 1018-1172 (Print) Linking ISSN: 10181172 NLM ISO Abbreviation: J Vasc Res Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Basel ; New York : S. Karger, c1992- |
| مواضيع طبية MeSH: | Blood Pressure*, Endothelium, Vascular/*physiopathology , Hyperhomocysteinemia/*physiopathology, Animals ; Aorta, Thoracic/physiopathology ; Body Weight ; Chronic Disease ; Dose-Response Relationship, Drug ; Hemodynamics ; Homocysteine/administration & dosage ; Homocysteine/blood ; Hyperhomocysteinemia/blood ; Hyperhomocysteinemia/chemically induced ; Male ; Mesenteric Arteries/physiopathology ; Rats ; Rats, Wistar ; Time Factors |
| مستخلص: | Mild hyperhomocysteinemia is prevalent in the general population and has been linked to endothelial dysfunction and high arterial pressure (AP) in clinical studies. The present study was designed to determine whether a rise in AP was induced by mild hyperhomocysteinemia and whether the potential rise in AP is secondary or prior to endothelial dysfunction. Experiments were performed in a rat model of mild hyperhomocysteinemia induced by oral administration of homocysteine for 1-4 months. Aortic endothelial dysfunction was observed 2 months after homocysteine treatment while endothelium-independent vasodilation was normal. In parallel, homocysteine treatment increased phenylephrine-induced contraction in aortas with endothelium, but did not modify the contraction in aortas without endothelium, suggesting a decrease of basal NO production. In conscious unrestrained rats, AP was not significantly different 1, 2, 3 and 4 months after homocysteine treatment. In correlation, endothelial function of a resistance vessel (mesenteric artery), mainly non-NO nonprostanoid factor mediated, was preserved, indicating that homocysteine treatment only affected the NO pathway. In conclusion, mild hyperhomocysteinemia alone is not sufficient to elevate arterial blood pressure, at least in the rat model. Aortic endothelial dysfunction produced by mild hyperhomocysteinemia is independent of hemodynamic factors. (Copyright 2005 S. Karger AG, Basel.) |
| المشرفين على المادة: | 0LVT1QZ0BA (Homocysteine) |
| تواريخ الأحداث: | Date Created: 20050217 Date Completed: 20050511 Latest Revision: 20131121 |
| رمز التحديث: | 20240628 |
| DOI: | 10.1159/000083972 |
| PMID: | 15713986 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1018-1172 |
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| DOI: | 10.1159/000083972 |