Journal article
Exercise improves the dilatation function of mesenteric arteries in postmyocardial infarction rats via a PI3K/Akt/eNOS pathway-mediated mechanism
American journal of physiology. Heart and circulatory physiology, Vol.299(6), pp.H2097-H2106
12/01/2010
DOI: 10.1152/ajpheart.00701.2010
PMID: 20935150
Abstract
Wang Y, Wang S, Wier WG, Zhang Q, Jiang H, Li Q, Chen S, Tian Z, Li Y, Yu X, Zhao M, Liu J, Yang J, Zhang J, Zang W. Exercise improves the dilatation function of mesenteric arteries in post-myocardial infarction rats via a PI3K/Akt/eNOS pathway-mediated mechanism. Am J Physiol Heart Circ Physiol 299: H2097-H2106, 2010. First published October 8, 2010; doi: 10.1152/ajpheart.00701.2010.-Myocardial infarction (MI) has been shown to induce endothelial dysfunction in peripheral resistance arteries and thus increase peripheral resistance. This study was designed to investigate the underlying mechanisms of post-MI-related dysfunctional dilatation of peripheral resistance arteries and, furthermore, to examine whether exercise may restore dysfunctional dilatation of peripheral resistance arteries. Adult male Sprague-Dawley rats were divided into three groups: sham-operated, MI, and MI + exercise. Ultrastructure and relaxation function of the mesenteric arteries, as well as phosphatidylinositol-3 kinase (PI3K), Akt kinases (Akt), endothelial nitric oxide synthase (eNOS) activity, and phosphorylation of PI3K, Akt, and eNOS by ACh were determined. Post-MI rats exhibited pronounced ultrastructural changes in mesenteric artery endothelial cells and endothelial dysfunction. In addition, the activities of PI3K, Akt, and eNOS, and their phosphorylation by ACh were significantly attenuated in mesenteric arteries (P < 0.05-0.01). After 8 wk of exercise, not only did endothelial cells appeared more normal in structure, but also ameliorated post-MI-associated mesenteric arterial dysfunction, which were accompanied by elevated activities of PI3K, Akt, and eNOS, and their phosphorylation by ACh (P < 0.05-0.01). Importantly, inhibition of either PI3K or eNOS attenuated exercise-induced restoration of the dilatation function and blocked PI3K, Akt, and eNOS phosphorylation by ACh in the mesenteric arteries. These data demonstrate that MI induces dysfunctional dilation of peripheral resistance arteries by degradation of endothelial structural integrity and attenuating PI3K-Akt-eNOS signaling. Exercise may restore dilatation function of peripheral resistance arteries by protecting endothelial structural integrity and increasing PI3K-Akt-eNOS signaling cascades.
Details
- Title: Subtitle
- Exercise improves the dilatation function of mesenteric arteries in postmyocardial infarction rats via a PI3K/Akt/eNOS pathway-mediated mechanism
- Creators
- Youhua Wang - Xi'an Jiaotong UniversityShengpeng Wang - Xi'an Jiaotong UniversityW. Gil Wier - University of Maryland, BaltimoreQuanjiang Zhang - Shaan Xi Normal Univ, Dept Phys Educ, Xian, Peoples R ChinaHongke Jiang - Xi'an Jiaotong UniversityQiuxia Li - Shaanxi Normal UniversityShengfeng Chen - Xi'an Jiaotong UniversityZhenjun Tian - Shaanxi Normal UniversityYouyou Li - Shaanxi Normal UniversityXiaojiang Yu - Xi'an Jiaotong UniversityMing Zhao - Xi'an Jiaotong UniversityJinjun Liu - Xi'an Jiaotong UniversityJing Yang - Xi'an Jiaotong UniversityJing Zhang - Xi'an Jiaotong UniversityWeijin Zang - Xi'an Jiaotong University
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.299(6), pp.H2097-H2106
- Publisher
- Amer Physiological Soc
- DOI
- 10.1152/ajpheart.00701.2010
- PMID
- 20935150
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Number of pages
- 10
- Grant note
- F510000/G16916404 / China Medical Board Distinguished Professorships Award 2007CB512005 / National Basic Research Program of China (973 Program); National Basic Research Program of China 30930105; 30873058; 30770785 / National Natural Science Foundation of China; National Natural Science Foundation of China (NSFC)
- Language
- English
- Date published
- 12/01/2010
- Academic Unit
- Cardiovascular Medicine; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984360158502771
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