title: [Effects of valsartan on myocardial calcium/calmodulin-dependent protein kinase-II expression and activity in a rabbit model of heart failure].
abstract: OBJECTIVE
  To investigate the effects of valsartan on myocardial expression and activity of calcium/calmodulin-dependent protein kinase-II (CaMK II) in a rabbit model of heart failure.
  
  
  METHODS
  Rabbits were divided into sham-operated group, heart failure group (volume overload by aortic valve destruction induced aortic insufficiency plus pressure overload induced by abdominal aortic banding) and heart failure plus valsartan (20 mg x kg(-1) x d(-1), n = 9 each). Seven weeks later, echocardiography and hemodynamic examinations were performed and myocardial CaMK II expression and activity were detected by Western blot and CaMK II activity assay kit, respectively.
  
  
  RESULTS
  Compared with the sham operated rabbits, left ventricular mass index [LVMI (3.61 +/- 0.09) g/kg vs. (1.32 +/- 0.06) g/kg, P<0.05] and end-diastolic pressure [LVEDP (23.00 +/- 2.37) mm Hg (1 mm Hg = 0.133 kPa) vs. (-1.50 +/- 0.5) mm Hg, P<0.05] were significantly increased while left ventricular shortening fractions [LVFS (17.38 +/- 3.13)% vs. (37.83 +/- 3.58)%, P<0.05] and ejection fraction [LVEF (38.50 +/- 6.07)% vs. (71.92 +/- 4. 56)%, P<0.05] were significantly decreased (all P<0.05) in heart failure rabbits, these changes could be significantly attenuated by valsartan treatment: LVMI [(2.07 +/- 0.14) g/kg vs. (3.61 +/- 0.09) g/kg, P<0.05], LVEDP [(2.17 +/- 0.72) mm Hg vs. (23.00 +/- 2.37) mm Hg, P<0.05], LVFS [(33.83 +/- 2.85)% vs. (17.38 +/- 3.13)%, P<0.05] and LVEF [(64.45 +/- 3.66)% vs. (38.50 +/- 6.07)%, P<0.05]. CaMK II expression (1.45 +/- 0.13 vs 0.89 +/- 0.05, 1.13 +/- 0.12, P<0.05) and activity [(3.54 +/- 0.17) pmol x min(-1) x microg(-1) vs. (2.18 +/- 0.13) pmol x min(-1) x microg(-1), (2.79 +/- 0.14) pmol x min(-1) x microg(-1), P<0.05] in heart failure rabbits were significantly increased than those sham operated rabbits which could be significantly attenuated by valsartan treatment.
  
  
  CONCLUSIONS
  Valsartan improved cardiac function in heart failure rabbits probably via downregulating myocardial CaMK II expression and activity.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Suzhou University, Suzhou 215006, China.
authors.forename: Fu-zheng
authors.initials: FZ
authors.lastname: Qu
authors.forename: Zhi-hua
authors.initials: ZH
authors.lastname: Liu
authors.forename: Bin
authors.initials: B
authors.lastname: Jiang
authors.forename: Cao
authors.initials: C
authors.lastname: Zou
authors.forename: Hong-xia
authors.initials: HX
authors.lastname: Li
authors.forename: Lian-hua
authors.initials: LH
authors.lastname: Han
authors.forename: Wen-ping
authors.initials: WP
authors.lastname: Jiang
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D011817:Rabbits; D013777:Tetrazoles / Q000627:therapeutic use*; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D013777:Tetrazoles; D000068756:Valsartan; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D014633:Valine; D002118:Calcium