| Effects of different levels of exercise volume on endothelium-dependent vasodilation: roles of nitric oxide synthase and heme oxygenase. | |
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MedLine Citation:
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PMID: 18633193 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The objective of this study was to examine the effects of moderate and high levels of exercise volume on endothelium-dependent vasodilation and associated changes in vascular endothelial/inducible nitric oxide synthase (eNOS and iNOS) and heme oxygenase (HO). Male Sprague-Dawley rats were assigned to sedentary control, acute (2 weeks), or chronic (6 weeks) treadmill running at moderate intensity (50% maximal aerobic velocity) with different durations of exercise episodes: 2 h/d (endurance training, moderate volume) and 3 h/d (intense training, high volume). Endothelium-dependent vascular function was examined in isolated thoracic aorta. Co-localization and contents of aortic eNOS/iNOS and HO-1/HO-2 were determined with immunofluorescence and Western blotting. Compared with sedentary controls, rats subjected to acute and chronic endurance training showed enhanced endothelium-dependent relaxation (p<0.01). Whereas acetylcholine-induced dilation was inhibited completely by NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) in sedentary controls, the dilation in the training groups was only partly blocked by L-NAME (inhibition was 98+/-3%, 79+/-6%, and 77+/-5% in sedentary control, acute, and chronic training groups, respectively, p<0.01). The remnant dilation in the training groups was further inhibited by HO inhibitor protoporphyrin IX zinc, with concomitant elevation in aortic eNOS as well as HO-1 and HO-2. In contrast to endurance exercise, high-volume intense training resulted in mild hypertension with significant impairment in endothelium-dependent vasodilation and profuse increases in aortic iNOS and eNOS (p<0.01). In conclusion, endothelium-dependent vasodilation is improved by endurance exercise but impaired by chronic intense training. Elevations of vascular eNOS and HO-1/HO-2 may contribute to enhanced vasodilation, which can be offset by intense training and elevation in vascular iNOS. |
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Authors:
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Meng-Wei Sun; Mei-Fang Zhong; Jun Gu; Feng-Lei Qian; Jian-Zhong Gu; Hong Chen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Hypertension research : official journal of the Japanese Society of Hypertension Volume: 31 ISSN: 0916-9636 ISO Abbreviation: Hypertens. Res. Publication Date: 2008 Apr |
Date Detail:
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Created Date: 2008-07-17 Completed Date: 2008-08-13 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 9307690 Medline TA: Hypertens Res Country: Japan |
Other Details:
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Languages: eng Pagination: 805-16 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R.China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aorta / enzymology Endothelium, Vascular / enzymology Heme Oxygenase (Decyclizing) / metabolism* Immunohistochemistry Male Nitrates / blood Nitric Oxide Synthase Type II / metabolism* Nitric Oxide Synthase Type III Nitrites / blood Physical Conditioning, Animal / physiology* Physical Exertion / physiology* Rats Rats, Sprague-Dawley Vasodilation / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Nitrates; 0/Nitrites; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos2 protein, rat; EC 1.14.13.39/Nos3 protein, rat; EC 1.14.99.3/Heme Oxygenase (Decyclizing); EC 1.14.99.3/Hmox1 protein, rat; EC 1.14.99.3/heme oxygenase-2 |
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