title: Effects of naturally acquired decompensated mitral valve regurgitation on the renin-angiotensin-aldosterone system and atrial natriuretic peptide concentration in dogs.
abstract: OBJECTIVE
  To investigate activity of the renin-angiotensin-aldosterone system and N-terminal pro-atrial natriuretic peptide (NT-proANP) during development of clinical signs of decompensated mitral valve regurgitation (MR).
  
  
  METHODS
  11 Cavalier King Charles Spaniels with advanced MR attributable to chronic valvular disease.
  
  
  METHODS
  Dogs were subjected to repeated examinations at 6-month intervals until signs of decompensation had developed (end point). Data acquired at end point were compared with data obtained from examinations 1 year and 1 to 6 months before decompensation. Each examination included physical examination, collection of venous blood, thoracic radiography, and echocardiography.
  
  
  RESULTS
  Echocardiographic measurements of left atrial-to-aortic root ratio and left ventricular end diastolic diameter increased considerably during the study, whereas left ventricular end systolic diameter remained unchanged. The increase in cardiac size was associated with increased plasma concentration of NT-proANP. In contrast, plasma concentrations of aldosterone and angiotensin II were reduced at decompensation (aldosterone compared with the 2 earlier examinations and angiotensin II compared with values obtained 1 to 6 months before), despite decreased plasma protein concentration and hematocrit, suggesting fluid retention. The urine-to-plasma creatinine ratio was reduced at end point.
  
  
  CONCLUSIONS
  Early decompensated MR in dogs was not associated with increased circulating renin-angiotensin-aldosterone system activity, which may be caused by increased activity of ANP, and may be important for future therapeutic strategies of MR.
authors.affiliation: Department of Physiology, Faculty of Veterinary Medicine, Faculty of Agriculture, University of Agricultural Sciences, Uppsala, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Häggström
authors.forename: K
authors.initials: K
authors.lastname: Hansson
authors.forename: C
authors.initials: C
authors.lastname: Kvart
authors.forename: B E
authors.initials: BE
authors.lastname: Karlberg
authors.forename: O
authors.initials: O
authors.lastname: Vuolteenaho
authors.forename: K
authors.initials: K
authors.lastname: Olsson
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood* / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D003404:Creatinine / Q000097:blood / Q000652:urine; D004283:Dog Diseases / Q000097:blood* / Q000503:physiopathology*; D004285:Dogs; D004452:Echocardiography / Q000379:methods / Q000662:veterinary; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology / Q000662:veterinary; D006400:Hematocrit; D008297:Male; D008944:Mitral Valve Insufficiency / Q000097:blood / Q000503:physiopathology / Q000662:veterinary*; D013902:Radiography, Thoracic / Q000379:methods / Q000662:veterinary; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D003404:Creatinine