title: Nitric oxide synthesis blockade reduced the baroreflex sensitivity in trained rats.
abstract: OBJECTIVE
  The present study has investigated the effect of blockade of nitric oxide synthesis on cardiovascular autonomic adaptations induced by aerobic physical training using different approaches: 1) double blockade with methylatropine and propranolol; 2) systolic arterial pressure (SAP) and heart rate variability (HRV) by means of spectral analysis; and 3) baroreflex sensitivity.
  
  
  METHODS
  Male Wistar rats were divided into four groups: sedentary rats (SR); sedentary rats treated with N(omega)-nitro-l-arginine methyl ester (L-NAME) for one week (SRL); rats trained for eight weeks (TR); and rats trained for eight weeks and treated with L-NAME in the last week (TRL).
  
  
  RESULTS
  Hypertension and tachycardia were observed in SRL group. Previous physical training attenuated the hypertension in L-NAME-treated rats. Bradycardia was seen in TR and TRL groups, although such a condition was more prominent in the latter. All trained rats had lower intrinsic heart rates. Pharmacological evaluation of cardiac autonomic tonus showed sympathetic predominance in SRL group, differently than other groups. Spectral analysis of HRV showed smaller low frequency oscillations (LF: 0.2-0.75 Hz) in SRL group compared to other groups. Rats treated with L-NAME presented greater LF oscillations in the SAP compared to non-treated rats, but oscillations were found to be smaller in TRL group. Nitric oxide synthesis inhibition with L-NAME reduced the baroreflex sensitivity in sedentary and trained animals.
  
  
  CONCLUSIONS
  Our results showed that nitric oxide synthesis blockade impaired the cardiovascular autonomic adaptations induced by previous aerobic physical training in rats that might be, at least in part, ascribed to a decreased baroreflex sensitivity.
authors.affiliation: Exercise Physiology Laboratory of the Department of Biomechanics, Medicine and Rehabilitation, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
authors.forename: Hugo C D
authors.initials: HC
authors.lastname: Souza
authors.forename: João E
authors.initials: JE
authors.lastname: De Araújo
authors.forename: Marli C
authors.initials: MC
authors.lastname: Martins-Pinge
authors.forename: Izabela C
authors.initials: IC
authors.lastname: Cozza
authors.forename: Daniel P
authors.initials: DP
authors.lastname: Martins-Dias
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001286:Atropine Derivatives / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology*; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004334:Drug Administration Schedule; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D010276:Parasympatholytics / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013057:Spectrum Analysis; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D001286:Atropine Derivatives; D004791:Enzyme Inhibitors; D010276:Parasympatholytics; D014665:Vasodilator Agents; D009569:Nitric Oxide; C006649:methylatropine; D011433:Propranolol; D019331:NG-Nitroarginine Methyl Ester