title: Downregulation of the vascular renin-angiotensin system by aerobic training - focus on the balance between vasoconstrictor and vasodilator axes - .
abstract: BACKGROUND
  Hyperactivity of the renin-angiotensin system (RAS) and functional deficits in hypertension are reduced after exercise training. We evaluate in arteries, kidney and plasma of hypertensive rats the sequential effects of training on vascular angiotensinogen, Ang II and Ang (1-7) content.
  
  
  RESULTS
  Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were trained or kept sedentary (S) for 3 months. After hemodynamic measurements (weeks 0, 1, 2, 4, 8 and 12), blood, arteries and kidneys were obtained to quantify the angiotensin content (HPLC) and angiotensinogen expression (Western Blotting). SHR-S vs. WKY-S exhibited elevated pressure, increased angiotensinogen and angiotensins' content in the renal artery with a high Ang II/Ang (1-7) ratio (~5-fold higher than in the femoral artery, kidney and plasma, and 14-fold higher than in the aorta). Training promptly reduced angiotensinogen expression and downregulated the RAS in the renal SHR artery (1st-12th week), with a specific reduction of the vasoconstrictor axis; significant reduction of the AngII/Ang (1-7) ratio (36%, T4-T8) occurred simultaneously with significant pressure fall (5%). In other SHR arteries, plasma and kidneys and in all WKY tissues, T-induced AngII and Ang (1-7) reductions were proportional, maintaining the AngII/Ang (1-7) ratio.
  
  
  CONCLUSIONS
  Vascular RAS is not equally expressed in vessels, having crucial importance in the renal artery. In the renal SHR artery, training downregulates the vasoconstrictor and preserves the vasodilator axis while in other tissues and plasma training reduces both RAS axes, thus maintaining the vasoconstriction/vasodilatation balance in a lower level.
authors: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo.
authors: Sebastião D
authors: SD
authors: Silva
authors: Thais T
authors: TT
authors: Zampieri
authors: Adriana
authors: A
authors: Ruggeri
authors: Alexandre
authors: A
authors: Ceroni
authors: Danielle S
authors: DS
authors: Aragão
authors: Fernanda B
authors: FB
authors: Fernandes
authors: Dulce E
authors: DE
authors: Casarini
authors: Lisete C
authors: LC
authors: Michelini
mesh_terms: D000332:Aerobiosis / Q000502:physiology; D000803:Angiotensin I / Q000096:biosynthesis* / Q000097:blood; D000804:Angiotensin II / Q000096:biosynthesis* / Q000097:blood; D000085962:Angiotensin-Converting Enzyme 2; D000808:Angiotensinogen / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D000818:Animals; D001794:Blood Pressure; D005263:Femoral Artery; D007668:Kidney / Q000378:metabolism*; D008297:Male; D009928:Organ Specificity; D010446:Peptide Fragments / Q000096:biosynthesis* / Q000097:blood; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012077:Renal Artery / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000502:physiology*; D012420:Running; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D010446:Peptide Fragments; D000808:Angiotensinogen; D000804:Angiotensin II; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; C000705329:Ace2 protein, rat; D000085962:Angiotensin-Converting Enzyme 2; C118790:angiotensin I (1-7)