New insights into the vascular mechanisms underlying the beneficial effect of swimming training on the endothelial vasodilator function in apolipoprotein E-deficient mice
| Autor: | Maxime Pellegrin, Vincent Gaume, Valérie Deckert, Christophe Houdayer, Alain Berthelot, Pascal Laurant |
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| Rok vydání: | 2007 |
| Předmět: |
Male
Apolipoprotein E medicine.medical_specialty Vascular smooth muscle Endothelium Vasodilator Agents Physical exercise Vasodilation Biology Nitric Oxide Muscle Smooth Vascular Mice Cyclic nucleotide chemistry.chemical_compound Apolipoproteins E Physical Conditioning Animal Internal medicine medicine Animals Nitric Oxide Donors Cyclic GMP Aorta Swimming Triglycerides Anatomy Atherosclerosis Acetylcholine Mice Mutant Strains Mice Inbred C57BL Hydrazines medicine.anatomical_structure Endocrinology chemistry lipids (amino acids peptides and proteins) Endothelium Vascular Cardiology and Cardiovascular Medicine Muscle Contraction medicine.drug Blood vessel |
| Zdroj: | Atherosclerosis. 190:35-42 |
| ISSN: | 0021-9150 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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