title: The renin-angiotensin system is modulated by swimming training depending on the age of spontaneously hypertensive rats.
abstract: OBJECTIVE
  To investigate the effects of swimming training on the renin-angiotensin system (RAS) during the development of hypertensive disease.
  
  
  METHODS
  Male spontaneously hypertensive rats (SHR) were randomized into: sedentary young (SY), trained young (TY), sedentary adult (SA), and trained adult (TA) groups. Swimming was performed 5 times/wk/8wks.
  
  
  RESULTS
  Trained young and adult rats showed both decreased systolic and mean blood pressure, and bradycardia after the training protocol. The left ventricular hypertrophy (LVH) was observed only in the TA group (12.7%), but there was no increase on the collagen volume fraction. Regarding the components of the RAS, TY showed lower activity and gene expression of angiotensinogen (AGT) compared to SY. The TA group showed lower activity of circulatory RAS components, such as decreased serum ACE activity and plasma renin activity compared to SA. However, depending on the age, although there were marked differences in the modulation of the RAS by training, both trained groups showed a reduction in circulating angiotensin II levels which may explain the lower blood pressure in both groups after swimming training.
  
  
  CONCLUSIONS
  Swimming training regulates the RAS differently in adult and young SHR rats. Decreased local cardiac RAS may have prevented the LVH exercise-induced in the TY group. Both groups decreased serum angiotensin II content, which may, at least in part, contribute to the lowering blood pressure effect of exercise training.
authors.affiliation: Hypertension Unit, Heart Institute (InCor), University of Sao Paulo Medical School, SP, Brazil.
authors.forename: F S
authors.initials: FS
authors.lastname: Zamo
authors.forename: V G
authors.initials: VG
authors.lastname: Barauna
authors.forename: S
authors.initials: S
authors.lastname: Chiavegatto
authors.forename: M C
authors.initials: MC
authors.lastname: Irigoyen
authors.forename: E M
authors.initials: EM
authors.lastname: Oliveira
mesh_terms: D000367:Age Factors; D000375:Aging / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000097:blood; D000809:Angiotensins / Q000097:blood / Q000235:genetics; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001919:Bradycardia / Q000503:physiopathology; D015870:Gene Expression; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D008297:Male; D009929:Organ Size; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D012084:Renin-Angiotensin System / Q000502:physiology*; D013550:Swimming / Q000502:physiology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000809:Angiotensins; D012333:RNA, Messenger; D007703:Peptidyl-Dipeptidase A