title: Renin-Angiotensin-aldosterone system and hypothalamic-pituitary-adrenal axis in hospitalized newborn foals.
abstract: BACKGROUND
  The renin-angiotensin-aldosterone system (RAAS) and hypothalamic-pituitary-adrenal axis (HPAA) and their interactions during illness and hypoperfusion are important to maintain organ function. HPAA dysfunction and relative adrenal insufficiency (RAI) are common in septic foals. Information is lacking on the RAAS and mineralocorticoid response in the context of RAI in newborn sick foals.
  
  
  OBJECTIVE
  To investigate the RAAS, as well as HPAA factors that interact with the RAAS, in hospitalized foals, and to determine their association with clinical findings. We hypothesized that critical illness in newborn foals results in RAAS activation, and that inappropriately low aldosterone concentrations are part of the RAI syndrome of critically ill foals.
  
  
  METHODS
  A total of 167 foals ≤3 days of age: 133 hospitalized (74 septic, 59 sick nonseptic) and 34 healthy foals.
  
  
  METHODS
  Prospective, multicenter, cross-sectional study. Blood samples were collected on admission. Plasma renin activity (PRA) and angiotensin-II (ANG-II), aldosterone, ACTH, and cortisol concentrations were measured in all foals.
  
  
  RESULTS
  ANG-II, aldosterone, ACTH, and cortisol concentrations as well as ACTH/aldosterone and ACTH/cortisol ratios were higher in septic foals compared with healthy foals (P < .05). No difference in PRA between groups was found. High serum potassium and low serum chloride concentrations were associated with hyperaldosteronemia in septic foals.
  
  
  CONCLUSIONS
  RAAS activation in critically ill foals is characterized by increased ANG-II and aldosterone concentrations. Inappropriately low cortisol and aldosterone concentrations defined as high ACTH/cortisol and ACTH/aldosterone ratios in septic foals suggest that RAI is not restricted to the zona fasciculata in critically ill newborn foals.
authors: Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH.
authors: K A
authors: KA
authors: Dembek
authors: K
authors: K
authors: Onasch
authors: S D A
authors: SD
authors: Hurcombe
authors: K C
authors: KC
authors: MacGillivray
authors: N M
authors: NM
authors: Slovis
authors: B S
authors: BS
authors: Barr
authors: S M
authors: SM
authors: Reed
authors: R E
authors: RE
authors: Toribio
mesh_terms: D000309:Adrenal Insufficiency / Q000097:blood / Q000503:physiopathology / Q000662:veterinary*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006734:Horse Diseases / Q000097:blood / Q000503:physiopathology*; D006736:Horses; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D008297:Male; D010913:Pituitary-Adrenal System / Q000502:physiology*; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000502:physiology*; D018805:Sepsis / Q000097:blood / Q000503:physiopathology / Q000662:veterinary*; D018709:Statistics, Nonparametric; D016019:Survival Analysis
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone