title: Early Spironolactone Treatment Attenuates  Heart Failure Development by Improving  Myocardial Function and Reducing Fibrosis  in Spontaneously Hypertensive Rats.
abstract: BACKGROUND
  We evaluated the role of the aldosterone blocker spironolactone in attenuating long-term pressure overload-induced cardiac remodeling and heart failure (HF) in spontaneously hypertensive rats (SHR).
  
  
  RESULTS
  Thirteen month-old male SHR were assigned to control (SHR-C, n=20) or spironolactone (SHR-SPR, 20 mg/kg/day, n=24) groups for six months. Normotensive Wistar-Kyoto rats (WKY, n=15) were used as controls. Systolic blood pressure was higher in SHR groups and unchanged by spironolactone. Right ventricular hypertrophy, which characterizes HF in SHR, was less frequent in SHR-SPR than SHR-C. Echocardiographic parameters did not differ between SHR groups. Myocardial function was improved in SHR-SPR compared to SHR-C [developed tension: WKY 4.85±0.68; SHR-C 5.22±1.64; SHR-SPR 6.80±1.49 g/mm2; -dT/dt: WKY 18.0 (16.0–19.0); SHR-C 20.8 (18.4–25.1); SHR-SPR 28.9 (24.2–34.6) g/mm2/s]. Cardiomyocyte cross-sectional area and total collagen concentration (WKY 1.06±0.34; SHR-C 1.85±0.63; SHR-SPR 1.28±0.39 μg/mg wet tissue) were greater in SHR-C than WKY and SHR-SPR. Type 3 collagen expression was lower in SHR-C than WKY and unchanged by spironolactone. Soluble collagen, type I collagen, and lysyl oxidase did not differ between groups.
  
  
  CONCLUSIONS
  Early spironolactone treatment decreases heart failure development frequency by improving myocardial systolic and diastolic function and attenuating hypertrophy and fibrosis in spontaneously hypertensive rats.
authors.forename: Marcelo D M
authors.initials: MD
authors.lastname: Cezar
authors.forename: Ricardo L
authors.initials: RL
authors.lastname: Damatto
authors.forename: Luana U
authors.initials: LU
authors.lastname: Pagan
authors.forename: Aline R R
authors.initials: AR
authors.lastname: Lima
authors.forename: Paula F
authors.initials: PF
authors.lastname: Martinez
authors.forename: Camila
authors.initials: C
authors.lastname: Bonomo
authors.forename: Camila M
authors.initials: CM
authors.lastname: Rosa
authors.forename: Dijon H S
authors.initials: DH
authors.lastname: Campos
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Cicogna
authors.forename: Mariana J
authors.initials: MJ
authors.lastname: Gomes
authors.forename: Silvio A
authors.initials: SA
authors.lastname: Oliveira
authors.forename: Daniella A
authors.initials: DA
authors.lastname: Blotta
authors.forename: Marina P
authors.initials: MP
authors.lastname: Okoshi
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
mesh_terms: D000818:Animals; D005355:Fibrosis; D006321:Heart / Q000187:drug effects*; D006333:Heart Failure / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D009206:Myocardium / Q000473:pathology*; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013148:Spironolactone / Q000627:therapeutic use*
chemical_list: D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone