title: Modulation of the tissue reninangiotensin-aldosterone system in dogs with chronic mild regurgitation through the mitral valve.
abstract: OBJECTIVE
  To investigate whether the tissue and plasma renin-angiotensin-aldosterone system (RAAS) is activated in dogs with mild regurgitation through the mitral valve and determine the contribution of chymase and angiotensin-converting enzyme (ACE) to the activation of the RAAS and potential production of angiotensin II during the chronic stage of mild mitral valve regurgitation.
  
  
  METHODS
  5 Beagles with experimentally induced mild mitral valve regurgitation and 6 clinically normal (control) Beagles.
  
  
  METHODS
  Tissue ACE and chymase-like activities and plasma RAAS were measured and the RAAS evaluated approximately 1,000 days after experimental induction of mitral valve regurgitation in the 5 dogs.
  
  
  RESULTS
  Dogs with experimentally induced mitral valve regurgitation did not have clinical signs of the condition, although echocardiography revealed substantial eccentric hyper- trophy. On the basis of these findings, dogs with mitral valve regurgitation were classified as International Small Animal Cardiac Health Council class Ib. Plasma activity of renin and plasma concentrations of angiotensin I, angiotensin II, and aldosterone were not significantly different between dogs with mitral valve regurgitation and clinically normal dogs. Tissue ACE activity was significantly increased and chymase-like activity significantly decreased in dogs with mitral valve regurgitation, compared with values in clinically normal dogs.
  
  
  CONCLUSIONS
  The tissue RAAS was modulated without changes in the plasma RAAS in dogs with mild mitral valve regurgitation during the chronic stage of the condition. An ACE-dependent pathway may be a major route for production of angiotensin II during this stage of the condition.
authors.affiliation: Department of Surgery, School of Veterinary Medicine, Azabu University, Kanagawa 229-8501, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Fujii
authors.forename: Kensuke
authors.initials: K
authors.lastname: Orito
authors.forename: Makoto
authors.initials: M
authors.lastname: Muto
authors.forename: Yoshito
authors.initials: Y
authors.lastname: Wakao
mesh_terms: D000818:Animals; D002908:Chronic Disease; D053818:Chymases / Q000378:metabolism; D004283:Dog Diseases / Q000201:enzymology / Q000503:physiopathology*; D004285:Dogs; D008944:Mitral Valve Insufficiency / Q000201:enzymology / Q000503:physiopathology / Q000662:veterinary*; D023421:Models, Animal; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D012016:Reference Values; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D007703:Peptidyl-Dipeptidase A; D053818:Chymases