Literature DB >> 28533932

Metabolic parameters and responsiveness of isolated iliac artery in LDLr-/- mice: role of aerobic exercise training.

Nádia F Garcia1, Amanda Cs Sponton2, Maria A Delbin2, Juliana M Parente3, Michele M Castro3, Angelina Zanesco4, Camila de Moraes1.   

Abstract

Physical inactivity and dyslipidemia are considered risk factors for cardiovascular diseases. There are few studies evaluating the effects of physical exercise in small-caliber artery in a model that mimics familial hypercholesterolemia. The aim of this study was to examine the effect of exercise training, at moderate intensity, on metabolic parameters and iliac artery responsiveness in LDL-/- mice. Sedentary (SD) and trained (TR) mice performed AET (5 days/week, 60 minutes/day at 60-70% of maximum speed) during 8 weeks. Body weight gain (BWG), epididymal fat, blood glucose, total cholesterol and triglycerides were evaluated. Concentration-response curves to acetylcholine (ACh), sodium nitroprusside, phenylephrine and U46619 were obtained in isolated iliac artery. The production of nitric oxide (NO) and reactive oxygen species as well as the expression and activity of MMP-2 were assessed. AET was effective in preventing BWG and epididymal fat gain, whereas no changes were observed in glucose, total cholesterol and triglycerides levels. Improvement in responsiveness to ACh was found in TR (Emax = 85±3%) compared with SD group (Emax = 62±5%) without changes in the maximal vascular response or potency to SNP, PHE and U46619. The NO level was increased (10.8-fold) while ROS formation was decreased (3.7-fold) in iliac artery from TR, without changes in MMP-2 activity or its expression. AET was effective to improve endothelium-dependent relaxation that was accompanied by increased NO production and decreased ROS formation in iliac artery. The intensity of AET should be greater to modify metabolic disorders in this experimental model of dyslipidemia.

Entities:  

Keywords:  Vascular reactivity; familial hypercholesterolemia; microvasculature; oxidative stress; physical exercise

Year:  2017        PMID: 28533932      PMCID: PMC5435607     

Source DB:  PubMed          Journal:  Am J Cardiovasc Dis        ISSN: 2160-200X


  27 in total

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