title: Parallel gene expressions of IL-6 and BNP during cardiac hypertrophy complicated with diastolic dysfunction in spontaneously hypertensive rats.
abstract: There is increasing evidence showing that inflammation is involved in heart failure. However, heart failure may differ greatly due to different aetiologies. The role of inflammation in hypertensive heart failure, particularly in the early stage of cardiac dysfunction, has not been studied completely. This study aims at finding out whether inflammation is involved in the early stage of heart dysfunction due to hypertension.
  
  
  METHODS
  Ten spontaneously hypertensive rats (SHR) and ten age-matched Wistar rats were used. Cardiac morphology and function, as well as coronary flow reserve, were examined by echocardiography. mRNAs for cytokines and brain natriuretic peptide were determined by RT-PCR.
  
  
  RESULTS
  The results demonstrate cardiac hypertrophy with increased heart/body weight ratio in SHR. Echocardiographic examination has shown that SHR developed diastolic heart dysfunction as determined by tissue Doppler without decrease in systolic function. In heart biopsies, there were increased mRNA levels for interleukin-6 and brain natriuretic peptide whereas decreased mRNA for interleukin-2, beta adrenergic receptor, interferon and NFkb in SHR as compared to WKY group. Coronary flow remained unchanged in both groups.
  
  
  CONCLUSIONS
  SHR developed cardiac hypertrophy complicated with diastolic heart dysfunction with increased expression of brain natriuretic peptide, down-regulation of beta adrenergic receptors and simultaneous up-regulation of IL-6, which indicates active proinflammatory process as, at least partly, underlying mechanism during the early stage when cardiac hypertrophy associated with diastolic dysfunction occurs.
authors.affiliation: Wallenberg Laboratory, Sahlgrenska University Hospital, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Espen.haugen@wlab.gu.se
authors.forename: E
authors.initials: E
authors.lastname: Haugen
authors.forename: J
authors.initials: J
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Wikström
authors.forename: J
authors.initials: J
authors.lastname: Grönros
authors.forename: L M
authors.initials: LM
authors.lastname: Gan
authors.forename: L X M
authors.initials: LX
authors.lastname: Fu
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D003971:Diastole; D004195:Disease Models, Animal; D004452:Echocardiography; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000209:etiology / Q000235:genetics*; D006973:Hypertension / Q000150:complications*; D006984:Hypertrophy; D015850:Interleukin-6 / Q000235:genetics*; D009206:Myocardium / Q000473:pathology; D020097:Natriuretic Peptide, Brain / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000235:genetics
chemical_list: D015850:Interleukin-6; D011943:Receptors, Adrenergic, beta; D020097:Natriuretic Peptide, Brain