title: Influence of aortic impedance on the development of pressure-overload left ventricular hypertrophy in rats.
abstract: BACKGROUND
  Aortic input impedance, which represents LV afterload, is considered to be a major determinant for the development of pressure-overload left ventricular (LV) hypertrophy.
  
  
  RESULTS
  To test whether the sustained change in aortic input impedance might affect the mode of development of LV hypertrophy, coarctation of either the ascending aorta (G1, n = 13) or suprarenal abdominal aorta (G2, n = 12) was performed over 4 weeks in 6-weeks-old Wistar rats. Although peak LV pressure and total systemic resistance were increased similarly in G1 and G2, time to peak LV pressure was decreased by 24% (P < .01) in G1 compared with G2. The aortic input impedance spectra revealed that the early systolic loading in G1 was characterized by an increase in characteristic impedance, whereas the late systolic loading in G2 was by an augmented arterial wave reflection. G1 showed a smaller increase (P < .01) in either the ratio of LV weight (mg) to body weight (g) or LV wall thickness than G2 after aortic banding. Myocyte diameter was also smaller (P < .05) in G1 (14.3 +/- 0.7 mm) than in G2 (16.1 +/- 1.2 mm). The ex vivo passive pressure-volume relation had a rightward shift in G1 compared with G2, suggesting less concentric LV hypertrophy in G1.
  
  
  CONCLUSIONS
  The sustained early systolic loading due to the increase in characteristic impedance was accompanied by less concentric, reduced hypertrophy, whereas the sustained late systolic loading due to the augmented arterial wave reflection was accompanied by concentric, adequate hypertrophy.
authors.affiliation: Second Department of Internal Medicine, Yamaguchi University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kobayashi
authors.forename: M
authors.initials: M
authors.lastname: Yano
authors.forename: M
authors.initials: M
authors.lastname: Kohno
authors.forename: M
authors.initials: M
authors.lastname: Obayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Hisamatsu
authors.forename: T
authors.initials: T
authors.lastname: Ryoke
authors.forename: T
authors.initials: T
authors.lastname: Ohkusa
authors.forename: K
authors.initials: K
authors.lastname: Yamakawa
authors.forename: M
authors.initials: M
authors.lastname: Matsuzaki
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001012:Aorta, Abdominal / Q000473:pathology / Q000503:physiopathology*; D001013:Aorta, Thoracic / Q000473:pathology / Q000502:physiology / Q000503:physiopathology*; D001017:Aortic Coarctation / Q000473:pathology / Q000503:physiopathology*; D001794:Blood Pressure; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values
chemical_list: D000804:Angiotensin II; D000450:Aldosterone