title: Influence of Valsartan on myocardial apoptosis in spontaneously hypertensive rats.
abstract: OBJECTIVE
  To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan.
  
  
  METHODS
  Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20 mg x kg(-1) x d(-1)) (SHR + Valsartan group), the others with placebo (SHR + placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay.
  
  
  RESULTS
  Mean blood pressure values were 127 +/- 2 mm Hg in controls, 163 +/- 6 mm Hg in the SHR + Valsartan group and 193 +/- 7 mm Hg in the SHR + placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175 +/- 3 mm Hg and 125 +/- 5 mm Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07 +/- 0.03 mg/g) and SHR + Valsartan groups (3.22 +/- 0.19 mg/g) compared with the SHR + placebo group (4.02 +/- 0.31 mg/g) (P < 0.05). The density of TUNEL-positive cells in Wistar and SHR +/- Valsartan groups was 23.3 +/- 3.3 nuclei/HPF and 35.0 +/- 1.3 nuclei/HPF, both of which were significantly less than that of the SHR + placebo group (116.7 +/- 11.3 nuclei/HPF).
  
  
  CONCLUSIONS
  In response to chronic pressure overload, cardiomyocyte-specific apoptosis contributes to the transition from compensatory hypertrophy to decompensation. Apoptosis may be effectively inhibited by Valsartan in the early stage of hypertension.
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. wml@public.hr.hl.cn
authors.forename: Weimin
authors.initials: W
authors.lastname: Li
authors.forename: Ningling
authors.initials: N
authors.lastname: Sun
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Chen
authors.forename: Youzhi
authors.initials: Y
authors.lastname: Yu
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D006332:Cardiomegaly / Q000473:pathology; D006973:Hypertension / Q000473:pathology*; D009206:Myocardium / Q000166:cytology*; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D013777:Tetrazoles / Q000494:pharmacology*; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology*; D000068756:Valsartan
chemical_list: D000959:Antihypertensive Agents; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine