title: Atrial natriuretic peptide property on the ischemic myocardium inducing HSP72.
abstract: BACKGROUND
  The purpose of this study was to investigate the effectiveness of atrial natriuretic peptide on ischemic myocardium through the induction of heat-shock protein 72.
  
  
  METHODS
  30 isolated rabbit hearts perfused on isolated heart apparatus were randomly assigned to receive either warm Krebs-Henseleit solution with 1 µmol L(-1) atrial natriuretic peptide (n = 15) or warm Krebs-Henseleit solution without atrial natriuretic peptide (n = 15) in preischemic, ischemic, and postischemic conditions. In all rabbit hearts, global ischemia was produced by clamping the aortic and atrial inflow lines. Concentrations of atrial natriuretic peptide were measured in hearts with left ventricular dysfunction following ischemia, and correlated with the hypertrophic growth sustained by overexpression of heat-shock protein 72 microRNA-133.
  
  
  RESULTS
  The levels of atrial natriuretic peptide were markedly higher in the group that received atrial natriuretic peptide, and strongly correlated with both band lengths of heat-shock protein 72 and overexpression of microRNA-133 in the hypertrophic myocyte.
  
  
  CONCLUSIONS
  Perfusion levels of atrial natriuretic peptide induce increased expression of heat-shock protein 72 microRNA-133 in dysfunctional left ventricle.
authors.affiliation: Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Italy.
authors.forename: Silvio
authors.initials: S
authors.lastname: Olivito
authors.forename: Massimo
authors.initials: M
authors.lastname: Chello
authors.forename: Elvio
authors.initials: E
authors.lastname: Covino
authors.forename: Pasquale
authors.initials: P
authors.lastname: Mastroroberto
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D002316:Cardiotonic Agents / Q000494:pharmacology*; D004195:Disease Models, Animal; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D035683:MicroRNAs / Q000378:metabolism; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010477:Perfusion; D011817:Rabbits; D013318:Stroke Volume / Q000187:drug effects; D013997:Time Factors; D015854:Up-Regulation; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D050884:HSP72 Heat-Shock Proteins; D035683:MicroRNAs; D009320:Atrial Natriuretic Factor
keywords: Atrial natriuretic factor; HSP72 heat-shock proteins; Hemodynamics; Hyperthermia; Myocardial reperfusion; induced