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

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Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_3F78674D39CC
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
New insights into the vascular mechanisms underlying the beneficial effect of swimming training on the endothelial vasodilator function in apolipoprotein E-deficient mice.
Périodique
Atherosclerosis
Auteur⸱e⸱s
Pellegrin M., Berthelot A., Houdayer C., Gaume V., Deckert V., Laurant P.
ISSN
0021-9150 (Print)
ISSN-L
0021-9150
Statut éditorial
Publié
Date de publication
01/2007
Peer-reviewed
Oui
Volume
190
Numéro
1
Pages
35-42
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
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.
Mots-clé
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
Création de la notice
23/08/2017 15:05
Dernière modification de la notice
09/05/2023 16:40
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