title: Aerobic exercise training increases nitrergic innervation function and decreases sympathetic innervation function in mesenteric artery from rats fed a high-fat diet.
abstract: BACKGROUND
  We investigated whether high-fat diet (HFD)-induced obesity was associated with modifications in mesenteric innervation function, the mechanisms involved, and the possible effects of aerobic exercise training on these changes.
  
  
  METHODS
  Male Wistar rats were divided into three groups: rats fed a standard diet (control group); rats fed a HFD (35% fat) for 8 weeks; and HFD rats submitted to aerobic exercise training (8 weeks, 5 times per week for 50  min). Segments of isolated mesenteric arteries were exposed to electric field stimulation (EFS) with or without phentolamine, suramin, or Nω nitro-L-arginine methyl ester. Noradrenaline, ATP, and nitric oxide release, and total and phosphorylated neuronal nitric oxide synthase (nNOS, P-nNOS) expression were also measured.
  
  
  RESULTS
  EFS contraction was greater in sedentary HFD than in control rats. Phentolamine reduced EFS contractions more markedly in HFD rats. Suramin decreased EFS contractions only in control rats. Phentolamine + suramin practically abolished EFS-induced contraction in control rats, whereas it did not modify it in the HFD rats. Noradrenaline release was greater and ATP was lower in HFD rats. Nω nitro-L-arginine methyl ester increased contractions to EFS only in segments from control rats. Nitric oxide release and nNOS and P-nNOS expressions were lower in arterial segments from HFD rats than from control rats. None of these changes in sedentary HFD rats was present in the trained HFD rats.
  
  
  CONCLUSIONS
  Enhanced sympathetic and diminished nitrergic components contributed to increased vasoconstrictor responses to EFS in sedentary HFD rats. All these changes were avoided by aerobic exercise training, suggesting that aerobic exercise could reduce peripheral vascular resistance in obesity.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid and Instituto de Investigación La Paz, IdIPAZ, Madrid, Spain *Esther Sastre and Laura Caracuel contributed equally to the writing of this article.
authors.forename: Esther
authors.initials: E
authors.lastname: Sastre
authors.forename: Laura
authors.initials: L
authors.lastname: Caracuel
authors.forename: Gloria
authors.initials: G
authors.lastname: Balfagón
authors.forename: Javier
authors.initials: J
authors.lastname: Blanco-Rivero
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D059305:Diet, High-Fat; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D026602:Nitrergic Neurons / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D009765:Obesity / Q000503:physiopathology*; D010646:Phentolamine / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013498:Suramin / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D013498:Suramin; D000255:Adenosine Triphosphate; D052248:Nitric Oxide Synthase Type I; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine; D010646:Phentolamine