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Effects of losartan potassium on myocardial mitochondrial proteins in spontaneously hypertensive rats with left ventricular hypertrophy

MENG Chao1, JIN Xian1, WANG Xiao-ling2, XIA Li2, CAI Jun3, FANG Ning-yuan1   

  1. 1.Department of Geriatrics, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200001, China; 2.Department of Pathophysiology, Basic Medicine Faculty of Shanghai Jiao Tong University, Shanghai 200025, China; 3.Pathology Center, Basic Medicine Faculty of Shanghai Jiao Tong University, Shanghai 200025, China
  • Online:2016-10-28 Published:2016-11-29
  • Supported by:

    Shanghai Pujiang Program, 14PJ1406300


Objective·To explore changes in myocardial mitochondrial proteinogram in spontaneously hypertensive rats (SHR) with left ventricular hypertrophy (LVH) and to investigate the effects of losartan potassium anti-hypertensive treatment on the proteinogram. Methods·20-week-old SHRs (SHR group) were randomly assigned to the 8-week losartan potassium anti-hypertensive treatment group (therapy group, 28-week-old) and the untreatment group (control group, 28-week-old). Wistar-Kyoto (WKY) rats aged 20 weeks were used as the controls of the SHR group (WKY group). Left ventricular mitochondrial proteinogram was measured using two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) combined with MALDI-TOF/TOF tandem mass spectrometry. Blood pressure and myocardial diameter of rats were also measured. Results·Thirteen mitochondrial protein spots showed alterations by more than 1.3 folds in the SHR group compared with the WKY group. Some spots were identified as the same protein by digestion and mass spectrometry analysis. Five identified proteins were all related to the energy metabolism of mitochondria. No additional different spots were identified after 8 weeks of anti-hypertensive treatment. The therapy group had significantly lower systolic blood pressure and diastolic blood pressure than the control group (P=0.000, P=0.002) and remarkably shorter myocardial diameter in enlarged left ventricles (P=0.000). Conclusion·SHRs with LVH have mitochondrial energy metabolism dysfunction. Losartan potassium can significantly decrease the blood pressure and partially reverse LVH, but has no significant effect on mitochondrial energy metabolism proteins, suggesting changes in mitochondrial proteins are possibly not caused by the load after hypertension.

Key words: mitochondrion, spontaneously hypertensive rats, left ventricular hypertrophy, losartan potassium, anti-hypertensive therapy