title: Acute changes of biventricular gene expression in volume and right ventricular pressure overload.
abstract: OBJECTIVE
  We investigated the effects of acute volume and RV pressure overload on biventricular function and gene expression of BNP, pro-inflammatory cytokines (IL-6 and TNF-alpha), iNOS, growth factors (IGF-1, ppET-1), ACE and Ca2+-handling proteins (SERCA2a, phospholamban and calsequestrin).
  
  
  METHODS
  Male Wistar rats (n=45) instrumented with pressure tip micromanometers in right (RV) and left ventricular (LV) cavities were assigned to one of three protocols: i) Acute RV pressure overload induced by pulmonary trunk banding in order to double RV peak systolic pressure, during 120 or 360 min; ii) acute volume overload induced by dextran40 infusion (5 ml/h), during 120 or 360 min; iii) Sham. RV and LV samples were collected for mRNA quantification.
  
  
  RESULTS
  BNP upregulation was restricted to the overloaded ventricles. TNF-alpha, IL-6, ppET-1, SERCA2a and phospholamban gene activation was higher in volume than in pressure overload. IGF-1 overexpression was similar in both types of overload, but was limited to the RV. TNF-alpha and CSQ mRNA levels were increased in the non-overloaded LV after pulmonary trunk banding. No significant changes were detected in ACE or iNOS expression. RV end-diastolic pressures positively correlated with local expression of BNP, TNF-alpha, IL-6, IGF-1, ppET-1 and SERCA2a, while RV peak systolic pressures correlated only with local expression of IL-6, IGF-1 and ppET-1.
  
  
  CONCLUSIONS
  Acute cardiac overload alters myocardial gene expression profile, distinctly in volume and pressure overload. These changes correlate more closely with diastolic than with systolic load. Nonetheless, gene activation is also present in the non-overloaded LV of selectively RV overloaded hearts.
authors.affiliation: Department of Physiology, Faculty of Medicine of Porto, Porto, Portugal.
authors.forename: Roberto
authors.initials: R
authors.lastname: Roncon-Albuquerque
authors.forename: Mariana
authors.initials: M
authors.lastname: Vasconcelos
authors.forename: André P
authors.initials: AP
authors.lastname: Lourenço
authors.forename: Ana
authors.initials: A
authors.lastname: Brandão-Nogueira
authors.forename: Antónia
authors.initials: A
authors.lastname: Teles
authors.forename: Tiago
authors.initials: T
authors.lastname: Henriques-Coelho
authors.forename: Adelino F
authors.initials: AF
authors.lastname: Leite-Moreira
mesh_terms: D000208:Acute Disease; D000818:Animals; D001685:Biological Factors / Q000235:genetics / Q000378:metabolism*; D003911:Dextrans / Q000008:administration & dosage; D004195:Disease Models, Animal; D015870:Gene Expression / Q000502:physiology*; D006352:Heart Ventricles / Q000378:metabolism*; D006439:Hemodynamics / Q000235:genetics; D008026:Ligation / Q000379:methods; D008297:Male; D040542:Mechanotransduction, Cellular / Q000235:genetics*; D032383:Myocytes, Cardiac / Q000502:physiology*; D011651:Pulmonary Artery / Q000601:surgery; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018497:Ventricular Dysfunction, Right / Q000235:genetics / Q000378:metabolism*; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D001685:Biological Factors; D003911:Dextrans; D012333:RNA, Messenger