title: Alterations in expression of sarcoplasmic reticulum gene in Dahl rats during the transition from compensatory myocardial hypertrophy to heart failure.
abstract: OBJECTIVE
  To clarify whether the functional changes during the transition from compensatory myocardial hypertrophy to failure are associated with changes in sarcoplasmic reticulum gene expression.
  
  
  METHODS
  We examined the gene expression of sarcoplasmic reticulum proteins [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, calsequestrin and ryanodine receptor] in Dahl salt-sensitive (Dahl-S) rats fed a high-salt (8%) diet from the age of 6 weeks. In-vivo contractile functioning was evaluated using echocardiography, and gene expression of sarcoplasmic reticulum proteins in the left ventricle was analyzed by Northern blotting for each stage of left ventricular hypertrophy.
  
  
  RESULTS
  SERCA messenger RNA (mRNA) levels in Dahl-S rats with compensatory hypertrophy did not change significantly, whereas phospholamban mRNA levels were increased by 61% (P < 0.01), and calsequestrin mRNA levels were increased by 130% (P < 0.01) compared with those in Dahl salt-resistant (Dahl-R) rats. SERCA mRNA levels in Dahl-S rats with decompensated dilatation were decreased by 32% (P< 0.05), whereas levels of phospholamban and calsequestrin mRNA remained unchanged. Ryanodine receptor mRNA levels did not change either with compensatory hypertrophy or with decompensated dilatation.
  
  
  CONCLUSIONS
  Alterations in expression of sarcoplasmic reticulum gene may be related to changes in systolic and diastolic properties in compensatory hypertrophy and heart failure.
authors.affiliation: Second Department of Internal Medicine, Ehime University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Okayama
authors.forename: M
authors.initials: M
authors.lastname: Hamada
authors.forename: H
authors.initials: H
authors.lastname: Kawakami
authors.forename: S
authors.initials: S
authors.lastname: Ikeda
authors.forename: H
authors.initials: H
authors.lastname: Hashida
authors.forename: Y
authors.initials: Y
authors.lastname: Shigematsu
authors.forename: K
authors.initials: K
authors.lastname: Hiwada
mesh_terms: D000818:Animals; D001794:Blood Pressure; D015152:Blotting, Northern; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000235:genetics / Q000378:metabolism; D002155:Calsequestrin / Q000235:genetics / Q000378:metabolism; D006332:Cardiomegaly / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004452:Echocardiography; D015870:Gene Expression; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D009200:Myocardial Contraction; D015345:Oligonucleotide Probes / Q000737:chemistry; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D019837:Ryanodine Receptor Calcium Release Channel / Q000235:genetics / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000235:genetics* / Q000378:metabolism*; D000099211:Phospholamban
chemical_list: D002135:Calcium-Binding Proteins; D000252:Calcium-Transporting ATPases; D002155:Calsequestrin; D015345:Oligonucleotide Probes; D012333:RNA, Messenger; D019837:Ryanodine Receptor Calcium Release Channel; D000099211:Phospholamban