title: Regulation of aortic extracellular matrix synthesis via noradrenergic system and angiotensin II in juvenile rats.
abstract: BACKGROUND
  Extracellular matrix (ECM) synthesis regulation by sympathetic nervous system (SNS) or angiotensin II (ANG II) was widely reported, but interaction between the two systems on ECM synthesis needs further investigation.
  
  
  OBJECTIVE
  We tested implication of SNS and ANG II on ECM synthesis in juvenile rat aorta.
  
  
  METHODS
  Sympathectomy with guanethidine (50 mg/kg, subcutaneous) and blockade of the ANG II AT1 receptors (AT1R) blocker with losartan (20 mg/kg/day in drinking water) were performed alone or in combination in rats. mRNA and protein synthesis of collagen and elastin were examined by Q-RT-PCR and immunoblotting.
  
  
  RESULTS
  Collagen type I and III mRNA were increased respectively by 62 and 43% after sympathectomy and decreased respectively by 31 and 60% after AT1R blockade. Combined treatment increased collagen type III by 36% but not collagen type I. The same tendency of collagen expression was observed at mRNA and protein levels after the three treatments. mRNA and protein level of elastin was decreased respectively by 63 and 39% and increased by 158 and 15% after losartan treatment. Combined treatment abrogates changes induced by single treatments.
  
  
  CONCLUSIONS
  The two systems act as antagonists on ECM expression in the aorta and combined inhibition of the two systems prevents imbalance of mRNA and protein level of collagen I and elastin induced by single treatment. Combined inhibition of the two systems prevents deposit or excessive reduction of ECM and can more prevent cardiovascular disorders.
authors.affiliation: Unité de Physiologie Intégrée, Laboratoire de Pathologies Vasculaires, Université de Carthage, Faculté des Sciences de Bizerte, Tunisia. houcine.dab@fsb.rnu.tn
authors.forename: Houcine
authors.initials: H
authors.lastname: Dab
authors.forename: Rafik
authors.initials: R
authors.lastname: Hachani
authors.forename: Nedra
authors.initials: N
authors.lastname: Dhaouadi
authors.forename: Mohsen
authors.initials: M
authors.lastname: Sakly
authors.forename: Wassim
authors.initials: W
authors.lastname: Hodroj
authors.forename: Jacques
authors.initials: J
authors.lastname: Randon
authors.forename: Giampiero
authors.initials: G
authors.lastname: Bricca
authors.forename: Kamel
authors.initials: K
authors.lastname: Kacem
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism*; D024042:Collagen Type I / Q000378:metabolism; D024043:Collagen Type II / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D004549:Elastin / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism*; D006145:Guanethidine / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D012333:RNA, Messenger; D051381:Rats; D011921:Rats, Inbred WKY; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013562:Sympathectomy / Q000379:methods; D013564:Sympathetic Nervous System / Q000378:metabolism*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D024042:Collagen Type I; D024043:Collagen Type II; D024061:Collagen Type III; D012333:RNA, Messenger; D000804:Angiotensin II; D004549:Elastin; D019808:Losartan; D006145:Guanethidine