title: Perivascular injury leads to a reduction in vascular reactivity of the collared and to an enhancement on contralateral carotid artery of rats.
abstract: BACKGROUND
  The first response to perivascular injury is observed in the adventitial layer. The purpose of this study was to determine the time course of vascular reactivity alterations after collar injury in rats. We also analyzed the relation between adventitial layer injury and vascular responsiveness to vasoconstrictor agents.
  
  
  METHODS
  Wistar rats had a silicone collar positioned around the carotid artery. The ipsilateral and contralateral arteries were morphologically analyzed 4, 7, 14 and 28 days after injury, and cumulative concentration-response curves to phenylephrine (Phe), angiotensin II (Ang II) and KCl were obtained for arteries isolated from collared and sham-operated groups.
  
  
  RESULTS
  Inflammatory cells and fibroblasts were observed in the adventitial layer of collared arteries 4, 7, 14 and 28 days after injury. Intimal thickening was observed in collared arteries only 14 and 28 days after perivascular injury. A decrease in maximum effect values (Emax) for Phe, Ang II and KCl was observed in the collared artery when compared with the contralateral artery at all times after injury, whereas an increase in vascular responsiveness was observed in the contralateral artery 4 days after injury.
  
  
  CONCLUSIONS
  The impairment of the contractile response preceded the intimal thickening. The compromise of vascular reactivity coincided with the presence of inflammatory cells and angiogenesis in the adventitial layer. The enhancement of the efficacy and potency of Ang II and Phe in collared-contralateral arteries 4 days after collar placement may be related to a receptor-mediated compensatory mechanism stimulated by the collar injury.
authors.affiliation: Department of Pharmacology, School of Medicine of Ribeirão Preto, USP, Ribeirão Preto SP, Brazil.
authors.forename: Sandra Y
authors.initials: SY
authors.lastname: Fukada
authors.forename: Fernando M A
authors.initials: FM
authors.lastname: Corrêa
authors.forename: Leandra N Z
authors.initials: LN
authors.lastname: Ramalho
authors.forename: Cristina I
authors.initials: CI
authors.lastname: Mizusaki
authors.forename: Ana M
authors.initials: AM
authors.lastname: de Oliveira
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D020212:Carotid Artery Injuries / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D003238:Connective Tissue / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D000804:Angiotensin II; D010656:Phenylephrine; D011189:Potassium Chloride