title: Hypertension induces compensatory arterial remodeling following arteriotomy.
abstract: BACKGROUND
  Hypertension has been traditionally considered a risk factor for restenosis following carotid arteriotomy. Genetic and morphological response to carotid arteriotomy in normotensive Wystar-Kyoto (WKY), spontaneously hypertensive (SHR), and Milan hypertensive (MHS) rats were analyzed.
  
  
  METHODS
  C-myc, angiotensin II receptor-1 (AT1), angiotensin II receptor-2 (AT2), endothelin-1 receptor A (ET(A)), endothelin-1 receptor B (ET(B)), Bcl-2 family-members (Bcl-2/Bax, Bcl-X(L/S)) were analyzed in surgically injured as well as uninjured carotids of WKY and hypertensive strains (HS). Thirty-day histology and morphometry were accomplished on injured and uninjured carotids.
  
  
  RESULTS
  C-myc mRNA is activated earlier and/or to a greater extent in hypertensive strains than in WKY. AT1 mRNA increases in WKY after injury, while it decreases in SHR and MHS. AT2 shows the opposite, decreasing in WKY and increasing in hypertensive strains. ET(A) mRNA decreases in all strains although with different timing and levels, associated with a replacement by ET(B) mRNA. Bcl-2/Bax ratio gradually decreases in WKY, while it shows only a transient decrease in SHR and MHS 4 h after the injury. Negative remodeling is observed in all injured carotids, although neointima was detected in WKY only. Thirty days following arteriotomy, morphometry demonstrated a significant decrease of luminal area, with consistent gain in the medial area in WKY, whereas hypertensive strains showed significant increase of the luminal area, consistent with a contemporary decrease of the medial area.
  
  
  CONCLUSIONS
  Vaso-relaxant AT2 and ET(B) induced limited vasoconstriction in HS. Less apoptosis in hypertensive rats reduced cell proliferation, contrasting c-myc. These responses favorably modulated media/lumen area ratio following arteriotomy in HS.
authors: Cardiac Surgery Unit Magna Graecia University of Catanzaro, Cantanzaro, Italy. frankono@libero.it
authors: Francesco
authors: F
authors: Onorati
authors: Amalia
authors: A
authors: Forte
authors: Pasquale
authors: P
authors: Mastroroberto
authors: Pasquale
authors: P
authors: Santè
authors: Salvatore
authors: S
authors: Esposito
authors: Francesco
authors: F
authors: Pezzo
authors: Lucio
authors: L
authors: Agozzino
authors: Marilena
authors: M
authors: Cipollaro
authors: Antonino
authors: A
authors: Cascino
authors: Attilio
authors: A
authors: Renzulli
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002339:Carotid Arteries / Q000502:physiology* / Q000601:surgery; D016893:Carotid Stenosis / Q000453:epidemiology / Q000503:physiopathology* / Q000601:surgery*; D015870:Gene Expression / Q000502:physiology; D006973:Hypertension / Q000453:epidemiology / Q000503:physiopathology*; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011945:Receptors, Angiotensin / Q000235:genetics; D017466:Receptors, Endothelin / Q000235:genetics; D012307:Risk Factors; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D011945:Receptors, Angiotensin; D017466:Receptors, Endothelin