title: Diet-induced obesity delays cardiovascular recovery from stress in spontaneously hypertensive rats.
abstract: OBJECTIVE
  Blood pressure (BP) and heart rate (HR) responses to stress are significant predictors of cardiovascular morbidity and mortality. Because obesity is a major risk factor for cardiovascular disease, we examined whether diet-induced obesity alters the BP and HR responses to stress and whether these alterations are associated with augmented cardiovascular morbidity in the rat.
  
  
  METHODS
  Adult male spontaneously hypertensive rats were fed either a normal diet or high-fat diet (HFD) for 12 weeks. At weeks 0 and 12, body weight was measured, and BP and HR were recorded by radiotelemetry throughout three consecutive day and night periods and in response to 30-minute immobilization stress. At the end of the 12-week intervention, the rats were sacrificed, and their organs and sera were collected.
  
  
  RESULTS
  With the intervention, HFD rats showed a significantly greater increase in body weight (as expected) and circulating leptin and free fatty acid levels compared with normal diet rats. In addition, they showed similar increases in BP and HR elevations during stress but significantly slower BP and HR decreases after stress. These HFD-induced delays in stress recovery were associated with BP and HR elevations during the night (behaviorally active) period and with augmentations in cardiac mass.
  
  
  CONCLUSIONS
  The results of this study indicate that, in spontaneously hypertensive rats, dietary obesity delays cardiovascular recovery from stress, and, in parallel, it promotes the development of nocturnal hypertension as well as cardiac hypertrophy. This suggests that dietary obesity may significantly potentiate the impact of daily stressful experiences on the cardiovascular system.
authors.affiliation: Centre de Recherche, Centre Hospitalier de l'Université de Montréal, Montréal, Canada.
authors.forename: Lucie
authors.initials: L
authors.lastname: Sedová
authors.forename: Julie
authors.initials: J
authors.lastname: Bérubé
authors.forename: Daniel
authors.initials: D
authors.lastname: Gaudet
authors.forename: Marc
authors.initials: M
authors.lastname: Dumont
authors.forename: Johanne
authors.initials: J
authors.lastname: Tremblay
authors.forename: Pavel
authors.initials: P
authors.lastname: Hamet
authors.forename: Zdenka
authors.initials: Z
authors.lastname: Pausová
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology*; D004041:Dietary Fats / Q000008:administration & dosage*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005951:Glucose Tolerance Test; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D007668:Kidney / Q000473:pathology; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D009206:Myocardium / Q000473:pathology; D009765:Obesity / Q000150:complications*; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000503:physiopathology*; D013997:Time Factors; D015430:Weight Gain
chemical_list: D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D020738:Leptin; D008055:Lipids