دورية أكاديمية

Vena cava presents endothelial dysfunction prior to thoracic aorta in heart failure: the pivotal role of nNOS uncoupling/oxidative stress.

التفاصيل البيبلوغرافية
العنوان: Vena cava presents endothelial dysfunction prior to thoracic aorta in heart failure: the pivotal role of nNOS uncoupling/oxidative stress.
المؤلفون: Dardi P; Department of Physiology and Biophysics, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, Brazil., Perazza LR; Department of Physiology and Biophysics, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, Brazil., Couto GK; Department of Physiology and Biophysics, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, Brazil., Campos GP; Department of Pharmacology, Institute of Biological Science, University of Minas Gerais, Minas Gerais, Brazil., Capettini LDSA; Department of Pharmacology, Institute of Biological Science, University of Minas Gerais, Minas Gerais, Brazil., Rossoni LV; Department of Physiology and Biophysics, Institute of Biomedical Science, University of Sao Paulo, Sao Paulo, Brazil.
المصدر: Clinical science (London, England : 1979) [Clin Sci (Lond)] 2021 Dec 10; Vol. 135 (23), pp. 2625-2641.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Portland Press on behalf of the Medical Research Society and the Biochemical Society Country of Publication: England NLM ID: 7905731 Publication Model: Print Cited Medium: Internet ISSN: 1470-8736 (Electronic) Linking ISSN: 01435221 NLM ISO Abbreviation: Clin Sci (Lond) Subsets: MEDLINE
أسماء مطبوعة: Publication: London : Portland Press on behalf of the Medical Research Society and the Biochemical Society
Original Publication: London, Medical Research Society.
مواضيع طبية MeSH: Aorta, Thoracic/*physiopathology , Endothelium, Vascular/*physiopathology , Heart Failure/*physiopathology , Nitric Oxide Synthase/*metabolism , Vena Cava, Inferior/*physiopathology, Animals ; Heart Failure/etiology ; Heart Failure/metabolism ; Hydrogen Peroxide/metabolism ; Male ; Myocardial Infarction/complications ; Oxidative Stress ; Rats, Wistar ; Vena Cava, Inferior/enzymology ; Rats
مستخلص: Arterial endothelial dysfunction has been extensively studied in heart failure (HF). However, little is known about the adjustments shown by the venous system in this condition. Considering that inferior vena cava (VC) tone could influence cardiac performance and HF prognosis, the aim of the present study was to assess the VC and thoracic aorta (TA) endothelial function of HF-post-myocardial infarction (MI) rats, comparing both endothelial responses and signaling pathways developed. Vascular reactivity of TA and VC from HF post-MI and sham operated (SO) rats was assessed with a wire myograph, 4 weeks after coronary artery occlusion surgery. Nitric oxide (NO), H2O2 production and oxidative stress were evaluated in situ with fluorescent probes, while protein expression and dimer/monomer ratio was assessed by Western blot. VC from HF rats presented endothelial dysfunction, while TA exhibited higher acetylcholine (ACh)-induced vasodilation when compared with vessels from SO rats. TA exhibited increased ACh-induced NO production due to a higher coupling of endothelial and neuronal NO synthases isoforms (eNOS, nNOS), and enhanced expression of antioxidant enzymes. These adjustments, however, were absent in VC of HF post-MI rats, which exhibited uncoupled nNOS, oxidative stress and higher H2O2 bioavailability. Altogether, the present study suggests a differential regulation of endothelial function between VC and TA of HF post-MI rats, most likely due to nNOS uncoupling and compromised antioxidant defense.
(© 2021 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)
فهرسة مساهمة: Keywords: Antioxidant Defense; Heart Failure; Oxidative Stress; Vena Cava; nNOS Uncoupling
المشرفين على المادة: BBX060AN9V (Hydrogen Peroxide)
EC 1.14.13.39 (Nitric Oxide Synthase)
تواريخ الأحداث: Date Created: 20211116 Date Completed: 20211216 Latest Revision: 20240226
رمز التحديث: 20240226
DOI: 10.1042/CS20210810
PMID: 34783347
قاعدة البيانات: MEDLINE
الوصف
تدمد:1470-8736
DOI:10.1042/CS20210810