New insights into the vascular mechanisms underlying the beneficial effect of swimming training on the endothelial vasodilator function in apolipoprotein E-deficient mice.

Details

Serval ID
serval:BIB_3F78674D39CC
Type
Article: article from journal or magazin.
Collection
Publications
Title
New insights into the vascular mechanisms underlying the beneficial effect of swimming training on the endothelial vasodilator function in apolipoprotein E-deficient mice.
Journal
Atherosclerosis
Author(s)
Pellegrin M., Berthelot A., Houdayer C., Gaume V., Deckert V., Laurant P.
ISSN
0021-9150 (Print)
ISSN-L
0021-9150
Publication state
Published
Issued date
01/2007
Peer-reviewed
Oui
Volume
190
Number
1
Pages
35-42
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
The antiatherogenic role of exercise is poorly understood. We examined the swimming exercise-induced vascular mechanisms which enhance the endothelial vasodilator function in apoE(-/-) mice. Male apoE(-/-) mice treated for 9 weeks with a lipid-rich diet were divided into two groups: the exercise group (apoE(-/-) X), which underwent a 9-week swimming protocol (50 min/day; 5days/week) and the sedentary group (apoE(-/-) S). C57BL/6 mice were used as the control group. Atherosclerotic lesions in the aortic roots were significantly reduced in apoE(-/-) X compared to apoE(-/-) S. Relaxation to acetylcholine was improved in apoE(-/-) X as compared to apoE(-/-) S and control mice with E(max) and pD(2) values significantly higher. pD(2) values in response to papaverine were higher in apoE(-/-) X than in the other groups. Relaxation in response to A23187 and DEA-NONOate were similar. These findings suggest that swimming training may increase the sensitivity of relaxation to acetylcholine, which in turn activates acetylcholine-mediated signaling pathways leading to increased NO bioactivity. Swimming may also prolong the signaling actions of NO by stimulating the sensitivity of vascular smooth muscle cells to cyclic nucleotides. These appear to be the key mechanisms underlying the improvement of the NO-cGMP pathway in exercised apoE(-/-) mice.

Keywords
Acetylcholine/pharmacology, Animals, Aorta/pathology, Aorta/physiology, Apolipoproteins E/deficiency, Apolipoproteins E/genetics, Atherosclerosis/pathology, Atherosclerosis/physiopathology, Atherosclerosis/prevention & control, Cyclic GMP/metabolism, Endothelium, Vascular/pathology, Endothelium, Vascular/physiology, Hydrazines/pharmacology, Male, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Muscle Contraction/drug effects, Muscle Contraction/physiology, Muscle, Smooth, Vascular/pathology, Muscle, Smooth, Vascular/physiology, Nitric Oxide/metabolism, Nitric Oxide Donors/pharmacology, Physical Conditioning, Animal/methods, Swimming, Triglycerides/blood, Vasodilation/drug effects, Vasodilation/physiology, Vasodilator Agents/pharmacology
Pubmed
Web of science
Create date
23/08/2017 16:05
Last modification date
20/08/2019 14:36
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