The effects of enalapril on p53 expression in left ventricular cardiomyocytes after aortic stenosis

In Vivo. 2006 Jul-Aug;20(4):459-65.

Abstract

ACE-inhibitors prevent the development of left ventricular hypertrophy (LVH). The tumor suppressor gene p53 up-regulates the cellular renin-angiotensin system, resulting in ANG II synthesis, which activates p53 creating a positive feedback loop. One hundred and fourteen rabbits were separated into groups A (control), B (sham-operated), C and D. In groups C and D, an aortic stenosis was performed, and in group D the animals were treated with enalapril. For p53 determination, LV specimens were examined by Western blot analysis and an immunohistochemical study was performed, except for samples from group D. In conclusion, LVH was significantly induced at 7 and 28 days after aortic stenosis with no difference between the two periods, while enalapril prevented hypertrophy in these two groups. p53 was transcriptionally activated and immunoreactively present after acute pressure overload as well as in the sham-operated group. Enalapril decreased the p53 expression at 180 min, 7 and 28 days following aortic stenosis.

Publication types

  • Comparative Study

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Animals
  • Aortic Valve Stenosis / complications*
  • Enalapril / pharmacology*
  • Heart Ventricles / cytology*
  • Hypertrophy, Left Ventricular / metabolism
  • Hypertrophy, Left Ventricular / prevention & control
  • Immunohistochemistry
  • Male
  • Myocytes, Cardiac / metabolism*
  • Rabbits
  • Time Factors
  • Tumor Suppressor Protein p53 / metabolism*
  • Ventricular Function, Left

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Tumor Suppressor Protein p53
  • Enalapril