title: Nitric oxide synthesis blockade increases hypertrophy and cardiac fibrosis in rats submitted to aerobic training.
abstract: OBJECTIVE
  The objective of the present study was to evaluate cardiac tissue adaptations in rats submitted to aerobic training after nitric oxide (NO) synthesis blockade.
  
  
  METHODS
  The animals (n=48) were divided into four groups: sedentary (CONTROL group); hypertensive after administration of NG-nitro-L-arginine methyl ester for 7 days (L-NAME Group); trained for 8 weeks through swimming exercises (TRAINED Group);trained and treated with L-NAME during the last week (L-NAME TRAINED Group). All the animals were submitted to the experiment procedures for blood pressure (BP) readings and cardiac morphometric evaluation.
  
  
  RESULTS
  In comparison to the other groups, the L-NAME and L-NAME TRAINED groups were hypertensive (p<0.05); however, BP elevation in the L-NAME TRAINED group was significantly lower than the L-NAME group (p<0.05). The heart weight indexes for the TRAINED and L-NAME TRAINED groups were higher than the CONTROL and L-NAME groups (p<0.05). Also they had presented higher rates of macroscopic cardiac area and cardiac fibrosis in relation to the rest (p<0.05); comparisons revealed that the values for the L-NAME TRAINED group were significantly higher (p<0.05) than the others.
  
  
  CONCLUSIONS
  Short term NO synthesis blockade in sedentary animals induced hypertension but did not cause cardiac hypertrophy. In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays an important role in cardiac tissue adaptations caused by aerobic exercise.
authors.affiliation: Faculdade de Medicina de Ribeirão Preto, Universidade Estadual de Londrina, Uberaba, MG, Brazil. hugocds@fmrp.usp.br
authors.forename: Hugo Celso Dutra de
authors.initials: HC
authors.lastname: Souza
authors.forename: Daniel Martins Dias
authors.initials: DM
authors.lastname: Penteado
authors.forename: Marli Cardoso
authors.initials: MC
authors.lastname: Martin-Pinge
authors.forename: Octávio
authors.initials: O
authors.lastname: Barbosa Neto
authors.forename: Vicente de Paula Antunes
authors.initials: Vde P
authors.lastname: Teixeira
authors.forename: João Henrique Dutra
authors.initials: JH
authors.lastname: Blanco
authors.forename: Valdo José Dias da
authors.initials: VJ
authors.lastname: Silva
mesh_terms: D000222:Adaptation, Physiological; D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D004719:Endomyocardial Fibrosis / Q000139:chemically induced / Q000473:pathology*; D004791:Enzyme Inhibitors; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase / Q000096:biosynthesis* / Q000502:physiology; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar; D013550:Swimming / Q000502:physiology
chemical_list: D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester