title: Cardiovascular changes during maturation and ageing in male and female spontaneously hypertensive rats.
abstract: BACKGROUND
  Cardiovascular remodeling leading to heart failure is common in the elderly. Testing effective pharmacological treatment of human heart failure requires a suitable animal model that adequately mimics the human disease state.
  
  
  METHODS
  This study has characterized the structural, functional, and electrical characteristics of the cardiovascular system throughout the lifespan in male and female spontaneously hypertensive rats (SHRs), a genetic model of chronic hypertension-induced cardiovascular remodeling, and age- and gender-matched normotensive controls, to determine whether ageing SHRs mimic the changes seen in ageing humans.
  
  
  RESULTS
  Both the ageing male and female SHRs developed progressive hypertension, ventricular hypertrophy, left ventricular fibrosis, action potential prolongation without impaired glucose tolerance. Male SHRs from 15 months of age exhibited left ventricular wall thinning and chamber dilation, together with systolic and diastolic dysfunction and increased cardiac stiffness and increased erythrocyte superoxide production, which were not present in the female SHRs.
  
  
  CONCLUSIONS
  Ageing male SHRs in contrast to the female SHRs, better mimic the chronic heart failure in humans produced by chronic hypertension. Ageing male SHRs could then be used to investigate proposed therapeutic interventions for chronic congestive heart failure in humans.
authors.affiliation: School of Biomedical Sciences, The University of Queensland, Brisbane, Australia.
authors.forename: Vincent
authors.initials: V
authors.lastname: Chan
authors.forename: Andrew
authors.initials: A
authors.lastname: Fenning
authors.forename: Scott P
authors.initials: SP
authors.lastname: Levick
authors.forename: David
authors.initials: D
authors.lastname: Loch
authors.forename: Prasad
authors.initials: P
authors.lastname: Chunduri
authors.forename: Abishek
authors.initials: A
authors.lastname: Iyer
authors.forename: Yi Ling
authors.initials: YL
authors.lastname: Teo
authors.forename: Andrew
authors.initials: A
authors.lastname: Hoey
authors.forename: Kathleen
authors.initials: K
authors.lastname: Wilson
authors.forename: Darryl
authors.initials: D
authors.lastname: Burstow
authors.forename: Lindsay
authors.initials: L
authors.lastname: Brown
mesh_terms: D000367:Age Factors; D000375:Aging; D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications*; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D012737:Sex Factors; D013045:Species Specificity; D013481:Superoxides / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D020257:Ventricular Remodeling
chemical_list: D013481:Superoxides