Document Detail


Effects of different levels of exercise volume on endothelium-dependent vasodilation: roles of nitric oxide synthase and heme oxygenase.
MedLine Citation:
PMID:  18633193     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Meng-Wei Sun; Mei-Fang Zhong; Jun Gu; Feng-Lei Qian; Jian-Zhong Gu; Hong Chen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
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:
Created Date:  2008-07-17     Completed Date:  2008-08-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9307690     Medline TA:  Hypertens Res     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  805-16     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R.China.
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MeSH Terms
Descriptor/Qualifier:
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:
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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