title: Angiotensin-converting enzyme inhibitor improves force and Ca2 +--frequency relationships in myocytes from rats with heart failure.
abstract: OBJECTIVE
  The objectives were to study the effects of an ACE inhibitor on the force-frequency relationship (FFR) and its possible mechanism in isolated failing myocytes.
  
  
  RESULTS
  Male Wistar rats were randomized into a heart failure group treated with perindopril (CHF-T, 3 mg.kg(-1)d-1), a heart failure group without treatment (CHF-C) and a sham-operated group (PS). Heart failure was induced by constriction of the abdominal aorta. All groups were further followed up for 12 weeks. Left ventricular myocytes were isolated. Cell-shortening fraction (FS) and intracellular calcium transients were measured at different frequency field stimulations. A negative force-frequency relationship (FFR) was found in the CHF-C group compared with the positive-negative biphasic FFR in the PS group, and a flat FFR in the CHF-T group. Intracellular Ca2+ frequency relationships (CaFRs) were positive-negative biphasic in both the PS and CHF-T groups, whereas a negative CaFR was found in the CHF-C group. Regardless of the stimulation frequency, FS significantly correlated with [Ca2+]imax in the PS or CHF-C groups. Compared to the PS group, protein levels of SERCA2 significantly decreased and NCX1 increased in the CHF-C group. In the CHF-T group, these changes were reduced.
  
  
  CONCLUSIONS
  The ACE inhibitor could improve the impaired FFR of isolated failing myocytes. This effect was possibly mediated via ameliorating the disturbance of CaFR.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
authors.forename: Xinxue
authors.initials: X
authors.lastname: Liao
authors.forename: Jiangui
authors.initials: J
authors.lastname: He
authors.forename: Hong
authors.initials: H
authors.lastname: Ma
authors.forename: Jun
authors.initials: J
authors.lastname: Tao
authors.forename: Wenfang
authors.initials: W
authors.lastname: Chen
authors.forename: Xiuyu
authors.initials: X
authors.lastname: Leng
authors.forename: Weiyi
authors.initials: W
authors.lastname: Mai
authors.forename: Wutao
authors.initials: W
authors.lastname: Zhen
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.forename: Lichun
authors.initials: L
authors.lastname: Wang
mesh_terms: D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000814:Aniline Compounds; D000818:Animals; D015153:Blotting, Western; D002135:Calcium-Binding Proteins / Q000187:drug effects / Q000378:metabolism*; D004195:Disease Models, Animal; D005456:Fluorescent Dyes; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D006352:Heart Ventricles / Q000166:cytology; D008297:Male; D018613:Microscopy, Confocal; D009200:Myocardial Contraction / Q000187:drug effects*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D020913:Perindopril / Q000494:pharmacology / Q000627:therapeutic use; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000187:drug effects / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger / Q000187:drug effects / Q000378:metabolism*; D014966:Xanthenes
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000814:Aniline Compounds; D002135:Calcium-Binding Proteins; D005456:Fluorescent Dyes; D019831:Sodium-Calcium Exchanger; D014966:Xanthenes; C059715:Fluo-3; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D020913:Perindopril